This paper presents an inhibitory learning approach to optimize exposure therapy for anxiety disorders. Exposure therapy is a mainstay of cognitive behavioral therapy for anxiety disorders, but many individuals do not benefit or experience a return of fear after treatment. Research suggests that anxious individuals show deficits in the mechanisms believed to underlie exposure therapy, such as inhibitory learning. The paper provides examples of how clinicians can apply an inhibitory learning model to optimize exposure therapy, distinguishing it from 'fear habituation' and 'belief disconfirmation' approaches. Exposure optimization strategies include expectancy violation, deepened extinction, occasional reinforced extinction, removal of safety signals, variability, retrieval cues, multiple contexts, and affect labeling. Case studies illustrate methods of applying these techniques with various anxiety disorders, including obsessive-compulsive disorder, posttraumatic stress disorder, social phobia, specific phobia, and panic disorder. The inhibitory learning model of extinction is central to exposure therapy. In a Pavlovian conditioning model, a neutral stimulus is followed by an aversive stimulus. After several pairings, the neutral stimulus elicits anticipatory fear. The CR is presumed to depend upon the CS becoming a reliable predictor of the US. An association is posited between the memory representations of the CS and the US such that presentations of the CS will indirectly activate the memory of the US. Fear conditioning is considered a valid model for many anxiety disorders. One powerful way to reduce conditional fear reactions is through extinction, in which the CS is repeatedly presented in the absence of the associated aversive event. Exposure therapy, wherein an individual is repeatedly exposed to fear provoking stimuli in the absence of repeated aversive outcomes, is the clinical proxy of extinction. Inhibitory learning is regarded as being central to extinction. Research into the neural mechanisms underlying fear extinction support an inhibitory model, since the amygdala, that is particularly active during fear conditioning, appears to be inhibited by cortical influences identified as occurring from the medial prefrontal cortex as a result of extinction learning. Bouton and colleagues propose that after extinction, the CS possesses two meanings; its original excitatory meaning (CS-US) as well as an additional inhibitory meaning (CS-noUS). Therefore, even though fear subsides with enough trials of the CS in the absence of the US, retention of at least part of the original association can be uncovered by various procedures, with each one showing a continuing effect of the original excitatory association after extinction. Deficits in inhibition and anxiety disorders are discussed. A substantial number of individuals fail to achieve clinically significant symptom relief from exposure-based therapies or experience a return of fear following exposure therapy. This may derive in part from the deficits in extinction learning and more specifically, deficits in inhibitory learning and inhibitory neural regulation during extinction, that characterize individuals with anxiety disorders or elevated trait anxiety. In other words, anxious individuals show deficits in the mechanisms that are believed to be central to extinction learning – such deficits may not only contribute to poor response toThis paper presents an inhibitory learning approach to optimize exposure therapy for anxiety disorders. Exposure therapy is a mainstay of cognitive behavioral therapy for anxiety disorders, but many individuals do not benefit or experience a return of fear after treatment. Research suggests that anxious individuals show deficits in the mechanisms believed to underlie exposure therapy, such as inhibitory learning. The paper provides examples of how clinicians can apply an inhibitory learning model to optimize exposure therapy, distinguishing it from 'fear habituation' and 'belief disconfirmation' approaches. Exposure optimization strategies include expectancy violation, deepened extinction, occasional reinforced extinction, removal of safety signals, variability, retrieval cues, multiple contexts, and affect labeling. Case studies illustrate methods of applying these techniques with various anxiety disorders, including obsessive-compulsive disorder, posttraumatic stress disorder, social phobia, specific phobia, and panic disorder. The inhibitory learning model of extinction is central to exposure therapy. In a Pavlovian conditioning model, a neutral stimulus is followed by an aversive stimulus. After several pairings, the neutral stimulus elicits anticipatory fear. The CR is presumed to depend upon the CS becoming a reliable predictor of the US. An association is posited between the memory representations of the CS and the US such that presentations of the CS will indirectly activate the memory of the US. Fear conditioning is considered a valid model for many anxiety disorders. One powerful way to reduce conditional fear reactions is through extinction, in which the CS is repeatedly presented in the absence of the associated aversive event. Exposure therapy, wherein an individual is repeatedly exposed to fear provoking stimuli in the absence of repeated aversive outcomes, is the clinical proxy of extinction. Inhibitory learning is regarded as being central to extinction. Research into the neural mechanisms underlying fear extinction support an inhibitory model, since the amygdala, that is particularly active during fear conditioning, appears to be inhibited by cortical influences identified as occurring from the medial prefrontal cortex as a result of extinction learning. Bouton and colleagues propose that after extinction, the CS possesses two meanings; its original excitatory meaning (CS-US) as well as an additional inhibitory meaning (CS-noUS). Therefore, even though fear subsides with enough trials of the CS in the absence of the US, retention of at least part of the original association can be uncovered by various procedures, with each one showing a continuing effect of the original excitatory association after extinction. Deficits in inhibition and anxiety disorders are discussed. A substantial number of individuals fail to achieve clinically significant symptom relief from exposure-based therapies or experience a return of fear following exposure therapy. This may derive in part from the deficits in extinction learning and more specifically, deficits in inhibitory learning and inhibitory neural regulation during extinction, that characterize individuals with anxiety disorders or elevated trait anxiety. In other words, anxious individuals show deficits in the mechanisms that are believed to be central to extinction learning – such deficits may not only contribute to poor response to