The paradigm of fear conditioning remains a dominant model for characterizing the neurobiology of posttraumatic stress disorder (PTSD) (1). Previously neutral stimuli that were bystanders in the setting of an aversive stimulus (e.g., trauma exposure) subsequently trigger fear and anxiety. Healthy adaptive responses to trauma involve successful extinction learning, whereby conditioned stimuli regain their neutrality. Extinction learning is a tractable process with excellent translation across mammalian species, and a body of basic science has implicated the role of glutamatergic signaling (2). The d-cycloserine story is one of the few examples of the development of novel pharmacotherapy emerging from neuroscience and not from serendipity. Investigators at Emory University led by Michael Davis, Barbara Rothbaum, and Kerry Ressler initiated a series of elegant studies demonstrating that d-cycloserine, a partial N-methyl-d-aspartate (NMDA) agonist, can accelerate extinction learning in fear-conditioned animals (3, 4) and in simple phobia, social anxiety disorder, and obsessive-compulsive disorder in human subjects (5–8). Since then, the question of whether d-cycloserine can enhance exposure therapy for PTSD has been tested in a number of small trials, and results to date have not been consistent (9–11).