Memory Reconsolidation: What Changes When Memories Are Reactivated
Author: Angela Bogdanova · Published: October 12, 2026 · Editorial Policy
Research cluster: Memory & Forgetting · Written by Artificial Sapiens
Memory reconsolidation describes a set of memory processes in which an established memory, after being reactivated under suitable conditions, becomes susceptible to modification and must undergo further stabilization. The central scientific question is whether reactivation opens a temporary period of neural plasticity in a previously consolidated memory representation. Experiments in animals strongly support this phenomenon in certain learning systems. Human research reports important compatible findings, together with replication failures and alternative explanations that limit generalization to complex personal memories.
The key distinction is between retrieving a memory and demonstrating reconsolidation. Remembering a past event does not automatically destabilize its neural representation, and changes in what someone reports after remembering do not, by themselves, establish that its original neural trace was rewritten. A critical review of human memory reconsolidation emphasizes the need for carefully controlled experiments before making that mechanistic inference.
This guide examines what researchers mean by reconsolidation, how they test it, what may determine whether a reactivated memory changes, what human experiments establish, and what claims about therapy, fear, personal memories, and memory editing remain unresolved.
What Is Memory Reconsolidation in Psychology?
Memory reconsolidation is the process by which a previously consolidated memory may require restabilization after reactivation. In a reconsolidation experiment, a reminder retrieves an established memory; under particular conditions the memory may enter a state of temporary instability, sometimes called lability or destabilization; processes involving neural plasticity then support its continued persistence or alteration. Research often operationalizes reconsolidation by showing that an intervention changes later memory performance when delivered after effective reactivation, but has a different effect without reactivation or outside the relevant temporal interval.
The definition has three components. The memory must already exist; the experimental manipulation must follow a reminder of that memory; and subsequent evidence must support a reactivation-dependent process rather than an ordinary change in response, newly learned association, or immediate retrieval ability. This is why the strongest studies compare multiple controls and delayed tests rather than simply asking whether a participant feels better after recalling something.
The broader term memory updating describes changes in a memory's content, strength, meaning, or accessibility as new information is encountered. Reconsolidation is one proposed neurobiological route through which such updating can occur. Updating can also arise through new learning, interference, integration, changed retrieval cues, inference, and reconstructed reporting. A 2017 review by Lee, Nader, and Schiller explains both the promise of the reconsolidation framework and the challenges involved in identifying its mechanism.
Reconsolidation, Consolidation, and Retrieval: Three Related Processes
Encoding is the initial processing of information encountered during an experience. Consolidation refers to changes through which a newly acquired memory becomes more stable and integrated over time. Retrieval is the later use of stored information: recalling a scene, recognizing a familiar voice, or responding to a learned signal. Reconsolidation concerns a possible further stabilization process following retrieval of an already established representation.
A student may learn a fact on Monday, remember it on Wednesday, and acquire a more precise explanation during that Wednesday review. The later knowledge could be integrated with the old representation, stored as additional learning, or used as a retrieval cue. Observing better understanding on Friday does not identify which neural mechanism produced the improvement. The same reasoning applies to emotional memories: reduced distress after a reminder may be meaningful without proving reconsolidation.
Initial consolidation and reconsolidation share some molecular themes, including activity-dependent neural plasticity, but they are not identical across all brain regions, species, tasks, or phases of learning. Consolidation itself includes multiple processes, from local synaptic changes to long-term reorganization among brain networks. Reconsolidation studies typically investigate the consequences of reactivation on specific learned representations. The distinctions are described in Schwabe, Nader, and Pruessner's review.
How Does Memory Reconsolidation Work?
Reactivation: retrieving a previously learned representation
A memory can be reactivated by a reminder that resembles an aspect of the original experience: a cue, context, sound, image, learned response, or instruction to recall. In the laboratory, researchers often establish a specific association on one day, present a reminder on another day, and measure retention later. A brief reminder is designed to bring the earlier association into play while limiting extensive new learning during the reminder itself.
Whether a given reminder reactivates the target representation in the needed way is a major experimental question. A cue that barely retrieves the memory may be ineffective; extensive repeated reminders may drive extinction, habituation, or a different kind of learning. Researchers therefore compare different reminder schedules and test how well participants learned the original material.
Destabilization: a conditional opening for change
The reconsolidation hypothesis proposes that some retrieved memories enter a temporary state in which changes can occur. Destabilization is a mechanistic inference, usually made from the selective vulnerability of reactivated memories to later intervention. It cannot ordinarily be observed directly by asking a person how vivid a memory feels.
Prediction error is one influential candidate for triggering destabilization. A reminder may create a mismatch between an expected event and what actually happens. For example, a learned cue predicts a particular consequence, but the consequence is omitted. In a human fear-conditioning experiment, Sevenster, Beckers, and Kindt (2013) reported that prediction error governed subsequent sensitivity to a pharmacological manipulation. Their follow-up work also explored the boundary between retrieval, reconsolidation, and new learning. The precise amount and nature of mismatch required depends on the paradigm; prediction error is a research variable rather than an everyday technique that guarantees a memory will become editable.
Restabilization: what happens after reactivation
Under reconsolidation accounts, neural processes re-establish a persistent representation after the period of vulnerability. Animal studies implicate protein synthesis and signaling pathways related to synaptic plasticity; other investigations explore changes in network activity and memory representation. Re-stabilization can coincide with apparent preservation, weakening, or strengthening of later performance. These outcomes are not equivalent to deleting a complete autobiographical event.
The idea of a fixed universal number of minutes during which any recalled memory can be rewritten is unsupported. Time windows used in experiments are determined by species, task, intervention, and the timing of memory tests. Conditions producing a result for a conditioned response cannot simply be prescribed for an ordinary human life event.
The Foundational Animal Experiment: Nader, Schafe, and LeDoux (2000)
A major turning point was the study Fear memories require protein synthesis in the amygdala for reconsolidation after retrieval. Rats first learned an association between a tone and an aversive event. After the association had been consolidated, researchers briefly reactivated the memory and infused the protein-synthesis inhibitor anisomycin into amygdala regions involved in this kind of conditioned fear learning.
Later performance was impaired when the drug followed appropriate retrieval. The intervention was less effective when the memory was not reactivated or when administration was delayed. This pattern offered evidence that a previously learned association could again become vulnerable to a molecular disruption after retrieval.
The result was important because it challenged a simple interpretation of consolidation as a single transition after which a learned representation could never again enter a vulnerable state. Its experimental precision also establishes its boundary: direct brain infusion of a protein-synthesis inhibitor in rodents is not a therapeutic procedure for humans, and a conditioned defensive response is not interchangeable with the narrative memory of an emotionally complex life event.
Subsequent animal research supports multiple forms of reactivation-dependent plasticity, while investigating why some memories resist destabilization, how reactivation interacts with extinction, and how molecular mechanisms differ between initial learning and later reactivation. The review of molecular mechanisms of reconsolidation-dependent updating situates the founding experiment within that more complicated literature.
What Human Experiments Have Found
Human fear-conditioning and reactivation-extinction procedures
Human participants can learn that a neutral visual stimulus predicts an uncomfortable but safe experimental outcome. Researchers measure changes in physiological conditioned responding, often through skin conductance, while varying when a reminder occurs and when extinction trials follow. Extinction is repeated experience of the cue without the anticipated consequence, which typically decreases the conditioned response.
Schiller and colleagues (2010) reported that extinction training conducted after a particular memory-reactivation interval helped prevent later recovery of conditioned fear. This became an influential demonstration of a possible behavioral reconsolidation-update procedure. Agren and colleagues (2012) reported changes in conditioned responding and amygdala-related imaging measures consistent with a reconsolidation interpretation, with an 18-month follow-up suggesting persistence in that particular paradigm.
These findings are scientifically important, but later investigations have challenged their reliability and interpretation. A registered direct replication in Cortex (2020) failed to find an advantage of the reactivation-extinction procedure over ordinary extinction. A separate verification report examining the original Schiller data found that the reported group differences depended substantially on discretionary participant exclusions. Therefore the 2010 experiment remains a landmark hypothesis-generating result, not a settled demonstration of a generally reproducible human intervention.
Propranolol and conditioned emotional responses
Propranolol is a beta-adrenergic receptor blocker used medically for several indications. Some experiments have administered it around the time of memory reactivation to investigate whether noradrenergic signaling contributes to subsequent emotional memory expression. Kindt, Soeter, and Vervliet (2009) reported attenuation of a conditioned fear response without comparable elimination of explicit knowledge of the learned association.
This distinction matters: emotional responding, conscious knowledge that two events were paired, and autobiographical recollection are separable outcomes. A change in one measurement does not certify deletion of every component of memory. In a 2022 systematic review and meta-analysis, the researchers identified 14 studies involving 478 healthy participants and 12 clinical studies involving 446 participants. The pooled findings favored propranolol-related reduction in some measured emotional-memory outcomes and symptoms, with variation in protocols and the quality of underlying evidence.
This experimental literature cannot justify unsupervised medication use or a general claim that propranolol erases personal memories. Medical decisions require attention to indications, contraindications, cardiovascular effects, drug interactions, and the evidence for the specific condition being treated. Clinical applications require their own controlled trials and guideline evaluation.
Declarative and episodic memory
Reconsolidation has also been investigated with facts, words, paired associates, scenes, and other consciously reportable material. In a 2007 human declarative-memory experiment, Forcato and colleagues studied how reactivation and subsequent interference related to later performance. Such experiments extend the research question beyond conditioned fear, yet interpreting them requires care because new information may interfere with earlier learning without altering the original stored representation.
The distinction between episodic and semantic memory also matters. Remembering a particular event includes its context, participants, temporal sequence, and meaning; recalling an experimental word association is a more constrained task. Laboratory evidence for one form of memory does not establish a universal mechanism for autobiographical memories accumulated across decades.
Procedural memory and motor skills
Reconsolidation-oriented research also includes skill and motor learning. A previously practiced movement can be reactivated and then tested after interference or stimulation. However, the outcome may reflect practice effects, performance fatigue, interference with a newly learned movement, or other aspects of plasticity. Studies must separate an immediate change in performance from a lasting change in what has been retained.
A 2026 systematic review of transcranial magnetic stimulation studies identified just five eligible human studies spanning fear, episodic, and procedural memory. Some outcomes were compatible with reconsolidation, but the evidence was heterogeneous and strongest in controlled laboratory paradigms. The authors did not establish a general-purpose method for editing naturalistic human memories.
Boundary Conditions: When Does Reactivation Lead to Reconsolidation?
Prediction error and surprise
An influential account holds that a memory is most likely to destabilize when reactivation reveals a meaningful discrepancy between what was learned and the current situation. The surprise must relate to the learned representation, and a mismatch can instead generate a separate new memory. The experimental prediction-error literature distinguishes brief reminders, memory destabilization, and more extensive new learning.
Surprise should not be treated as a magic ingredient. Studies differ in how expectations are formed, how mismatch is induced, and how destabilization is inferred. Some experiments show effects in the absence of obvious subjective surprise; others report null results despite procedures that appear to contain a mismatch.
Memory strength, age, and prior training
Older or strongly reinforced memories can be more resistant to particular post-retrieval interventions in some paradigms. Yet strength and age do not form absolute barriers across all experimental systems. Repetition, emotional intensity, the person's existing knowledge, and the relevance of the reminder may interact with the design. A review of research on strong and old memories cautions against turning proposed boundary conditions into universal laws.
A highly rehearsed childhood memory is therefore neither necessarily permanently fixed nor necessarily susceptible to a particular reconsolidation intervention. Strong autobiographical memories are networks of details, beliefs, interpretations, and emotional responses accumulated through many retrievals and later experiences.
Duration and quality of the reminder
A reminder can be too weak to retrieve the intended association effectively. Extended cue presentations can induce extinction or additional learning. The interval before a subsequent task matters experimentally, but different protocols can produce competing mechanisms. The same procedure may behave differently in participants who learned the original association at different strengths.
For this reason a study should report its acquisition criteria, timing, reminder exposures, retention tests, exclusions, and analysis plan. Broad clinical claims based solely on the presence of a brief recall exercise omit the variables that make a reconsolidation claim testable.
Stress, emotion, and context
Emotional arousal and stress hormones can influence encoding, retrieval, and later memory expression, but their effects vary with intensity and timing. Social setting and perceived safety can also change how a person responds to reminders. Some relevant findings arise from specific fear-conditioning and pharmacological paradigms; they do not imply that every emotionally intense recollection enters the same neurobiological state.
The responsible conclusion is that reconsolidation is conditional. Its boundary conditions remain a central research problem rather than a completed universal recipe.
How Can Scientists Tell Whether Reconsolidation Occurred?
A convincing study first establishes and measures the original learning, waits long enough to study an established memory, and manipulates retrieval rather than only comparing different new-learning conditions. It then includes a reactivation group and a no-reactivation comparison, alongside suitable intervention and control groups.
Timing controls ask whether the intervention matters within the proposed post-reactivation period. Delayed tests ask whether the result persists beyond an immediate effect on arousal, attention, or motor performance. Multiple forms of measurement can separate explicit recognition, spontaneous recall, conditioned physiological responding, self-report, and functional behavior. Independent replication and preregistered analysis plans are especially valuable when findings are sensitive to exclusions or complex statistical choices.
A key challenge is what researchers call the alternative-explanation problem. A participant may display less fear because the old association was modified, a new safety association was learned, attention to the cue changed, or the test itself altered responding. The observable result alone often fits several explanations. Elsey, Van Ast, and Kindt's critical human framework highlights how difficult it is to prove a reconsolidation mechanism with behavioral evidence alone.
Brain imaging adds information about neural activity and connectivity, but changes in a measured signal cannot by themselves prove that a specific autobiographical memory has been erased. Experimental controls, convergence across methods, and explicit model comparison are required.
Memory Reconsolidation Versus Extinction, Interference, and Reconstruction
Extinction refers to a decline in a learned response when the cue occurs without the expected outcome. Many accounts emphasize new inhibitory learning that can coexist with earlier learning, which helps explain why a response can sometimes return after delay, context change, or further stimulation. Reconsolidation-based theories propose that some reactivation-linked interventions alter an earlier representation more directly. Distinguishing these mechanisms experimentally remains difficult.
Interference occurs when competing information changes how efficiently material is retrieved or remembered. A newly learned list might impair recall of an older list. This need not entail molecular destabilization of the older memory. Reconsolidation experiments with verbal material therefore require controls for ordinary interference.
Reconstructive memory refers to the way remembering uses retained information together with current knowledge, inference, context, and suggestion. A person may tell the story of an event differently after seeing new evidence. That is a real psychological change, but the same report cannot establish whether the original representation underwent reconsolidation. For the dedicated explanation of post-event suggestion, see our English article on the misinformation effect in eyewitness memory.
Reappraisal involves reconsidering the meaning of an event. Someone may continue to remember a public-speaking mistake while coming to view it as ordinary and survivable. That change may improve emotional functioning, even when no experiment has identified the underlying reconsolidation pathway.
Does Reconsolidation Mean That Memories Can Be Erased?
The term erasure has been used in titles and interpretations of some experiments, particularly when a conditioned response or its measured neural correlate was greatly reduced. In these studies, the outcome is usually defined for a narrow learned association and particular performance or imaging measure. The absence of a measured response at a later test does not demonstrate that every component of the original experience has vanished from every memory system.
A human autobiographical memory often contains an episodic narrative, semantic knowledge, emotional appraisal, bodily associations, social accounts, and cues linked to many other experiences. Reducing physiological fear of a laboratory cue is a different achievement from deleting a detailed episode from a person's personal history.
The responsible scientific language distinguishes attenuation of response, changes in later retrieval, durable behavioral updating, and demonstrated neural reconsolidation. The phrase permanent memory deletion exceeds what contemporary evidence ordinarily establishes for complex personal memories. Even a large improvement in distress does not verify historical accuracy or determine how an individual's recollection is represented in the brain.
Can Memory Reconsolidation Help in Psychotherapy?
Reconsolidation is scientifically relevant to psychotherapy because many treatments involve recalling emotionally important material, learning new meanings, and responding differently to reminders. Researchers have investigated whether a carefully timed reactivation and updating procedure can reduce fear, craving, or other problematic responses. A clinical review in Annual Review of Clinical Psychology describes the appeal of this approach together with mixed translation results.
A therapy can have demonstrated benefits even when its neural mechanism remains uncertain. Conversely, a persuasive description of memory reconsolidation does not establish that a particular proprietary technique is clinically effective. Therapeutic effectiveness requires controlled outcomes relevant to the clinical condition, meaningful follow-up, replication, safety assessment, and comparison with established care.
For posttraumatic stress disorder, the NICE PTSD guideline recommends specific trauma-focused psychotherapies, including trauma-focused cognitive behavioral therapies and eye movement desensitization and reprocessing in specified circumstances. That recommendation is based on clinical evidence for the interventions. It should not be relabeled as proof that each successful treatment works by reconsolidation.
The English Hub's detailed trauma and memory article addresses intrusive recall, memory gaps, and the clinical boundaries of PTSD-related memory claims. Its clinical search intent remains distinct from the present article's focus on experimental reconsolidation mechanisms.
What about reconsolidation-focused techniques advertised online?
Commercial programs may describe a brief sequence of recalling a painful experience, introducing a contradictory experience, and permanently neutralizing the old memory. Such a description resembles a possible mechanistic hypothesis but does not substitute for evidence from the advertised program's own trials. Different therapies can contain similar ingredients while differing dramatically in implementation and outcomes.
Readers should ask which specific problem was studied, which outcomes improved, whether randomized comparisons exist, how long benefits lasted, what adverse effects were recorded, and whether independent investigators replicated the results. Testimonials, clinical case reports, and claims of an opened memory window offer different and generally weaker forms of evidence than well-designed controlled trials.
A person experiencing substantial symptoms should seek assessment from an appropriately qualified clinician. Recall exercises designed to provoke overwhelming distress are not a substitute for individualized care.
Can Reconsolidation Change Memories of Trauma or Addiction?
There is preliminary and developing research on interventions targeting emotionally salient associations in PTSD, addiction, phobias, and related conditions. Laboratory cue memories, patient-specific emotional reactions, craving, symptom severity, and quality of life are different outcomes. A study showing reduced skin conductance during a learned laboratory cue does not prove treatment of PTSD, and clinical symptom improvement does not prove erasure of an original memory.
The 2022 propranolol meta-analysis found pooled benefits across selected healthy and clinical samples, but differences in the interventions, patient groups, study designs, and outcomes make general clinical recommendations premature. Reviews emphasize that reconsolidation findings need to be evaluated in real-world treatment settings separately from established therapies.
A traumatic memory may be recalled accurately, incompletely, or reconstructively; reconsolidation science does not provide a test of its historical truth. Likewise, a memory that feels newly recovered during treatment needs careful handling because confidence, vividness, and clinical interpretation do not independently verify an event.
Does Remembering Something Repeatedly Change It?
Repeated remembering can change later memory performance, emotional response, and the organization of a personal story. Rehearsal may strengthen access to selected details; updated knowledge may alter interpretations; suggestion may increase particular errors; repeated retrieval may also make some facts easier to recall. Those outcomes reflect several ordinary learning and remembering processes.
Reconsolidation is one candidate mechanism under suitable conditions. There is no evidence that every retrieval causes a complete period of destabilization, and no universal rule that a memory becomes less accurate each time it is recalled. Some details remain highly stable across repeated remembering; others become more accessible, less accessible, or reorganized.
In everyday life the useful distinction is between a memory's subjective vividness, its factual accuracy, its emotional significance, and the mechanisms responsible for later changes. These dimensions can move independently. A person may become less upset about a remembered event while retaining its essential details.
Individual Differences, Development, and the Limits of Generalization
Much controlled human reconsolidation research uses adults in laboratory settings. Results may vary by previous learning history, context, medications, arousal, age, and how strongly a cue retrieves the original information. The scientific literature remains too heterogeneous to prescribe one reactivation procedure for all individuals.
Developmental changes in memory, aging, and clinical conditions create further questions. A result in young adult volunteers should not be generalized automatically to children, older adults, or people living with complex medical or psychiatric conditions. Memory complaints require attention to sleep, stress, medications, health, and daily functioning; reconsolidation does not operate as a diagnostic test.
Sleep also supports memory reactivation and consolidation, but sleep-related replay and experimentally induced post-retrieval reconsolidation are distinct research problems. The English Hub's sleep and memory guide addresses the separate question of how sleep affects remembering.
The State of the Evidence in 2026
Established evidence supports the principle that already acquired memories are dynamic and that, in certain animal learning paradigms, reactivation-dependent vulnerability can be demonstrated experimentally. This is the strongest mechanistic foundation of the field.
Human studies provide a substantial but mixed body of results consistent with reconsolidation in selected emotional, declarative, and procedural tasks. Some experiments show lasting changes in later responses. However, inconsistent replication, intervention heterogeneity, contested analytic decisions in influential studies, and viable alternative mechanisms constrain what can be concluded about specific neural processes. The 2018 human critical review and 2020 registered replication remain especially important for interpreting stronger popular claims.
The 2026 systematic review of TMS and reactivation illustrates both continued progress and the small, heterogeneous evidence base for emerging intervention approaches. It found five qualifying human investigations and concluded that post-reactivation modulation was most convincingly supported in carefully controlled laboratory settings.
Clinical applications are active research targets. Individual interventions may show promise, but claims about guaranteed permanent erasure of harmful memories, universal reconsolidation windows, or a single psychological technique that rewrites personal history remain unsupported. Progress will depend on reliable boundary-condition tests, mechanistic converging evidence, preregistration, independent replications, and patient-centered outcomes.
Frequently Asked Questions
What is a simple example of memory reconsolidation?
In a laboratory, a participant learns an association, encounters a reminder after the association has become established, and then undergoes an intervention. If later retention changes specifically because of the reminder and its timing, the result can support reconsolidation. A person simply reconsidering a past mistake is an example of psychological memory updating, but not proof of reconsolidation.
Does recalling a memory make it unstable?
Sometimes under experimentally defined conditions. Retrieval is a necessary part of typical reconsolidation designs, but ordinary recall does not guarantee measurable destabilization. The kind of reminder, prediction error, learning history, and test procedures all matter.
How long is the reconsolidation window?
Experimental windows depend on the learning system and method. Research sometimes applies interventions minutes or hours after reactivation, but there is no validated universal duration that applies to every human memory. The timing of a particular study must be interpreted within its protocol.
Can you intentionally rewrite an old memory?
People can acquire new interpretations, associations, and contextual knowledge, and some laboratory studies report post-reactivation changes in specific memory outcomes. There is no generally validated technique for precisely editing or deleting a chosen complex autobiographical memory.
Is memory reconsolidation scientifically proven?
Reactivation-dependent plasticity is strongly supported in some animal paradigms. Human findings are substantial but mixed, and proving a specific reconsolidation mechanism from an observed change in performance is difficult. Claims of broad clinical memory erasure exceed the current evidence.
What is the difference between reconsolidation and extinction?
Extinction is reduced responding following experiences that violate an expected outcome and often involves new inhibitory learning. Reconsolidation proposes a restabilization phase in an existing representation after reactivation. Some procedures may engage both processes, and experiments must distinguish them rather than infer one from a decline in fear.
Does reconsolidation explain false memories?
It may contribute to some updating, but false memories can arise through suggestion, source-monitoring errors, inference, and reconstruction. A false report does not automatically establish neural reconsolidation. The mechanisms are distinct research questions.
Can propranolol erase a traumatic memory?
Evidence supports changes in some conditioned emotional responses under particular protocols. It does not establish reliable deletion of personal traumatic events, and propranolol requires medical assessment rather than self-experimentation.
Does EMDR work by reconsolidation?
EMDR has a clinical evidence base for PTSD, but attributing its benefits specifically to reconsolidation requires separate mechanistic evidence. A therapy's demonstrated benefit and an explanation of how it works are distinct claims.
What would count as definitive evidence of reconsolidation in humans?
A persuasive body of evidence would combine reactivation and timing controls, durable changes in defined memory outcomes, clear separation from new learning and retrieval effects, appropriate neural evidence, and independent replication across research teams. No single subjective memory report settles the mechanism.
Can reconsolidation improve memory instead of weakening it?
Some experiments investigate strengthening or updating following retrieval, in addition to weakening. Whether an intervention enhances later performance depends on the memory system and study conditions. The possibility does not validate commercial brain-training or memory enhancement guarantees.
Is memory reconsolidation the same as memory consolidation?
Consolidation usually refers to stabilization after initial acquisition; reconsolidation concerns possible restabilization after an established memory has been reactivated. They can share components while differing in timing, requirements, and experimental evidence.
Related Articles
For related processes in a separate English Hub cluster, read Sleep and Memory: Consolidation, Learning, and Sleep Loss. For experimentally distinct distortions in eyewitness remembering, explore The Misinformation Effect in Eyewitness Memory. For PTSD-related clinical memory questions, see Trauma and Memory: Intrusive Memories, Gaps, and Evidence.
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