Dr. Gray criticizes the article for omitting reference to earlier articles by him and his colleagues, most prominent among them the article in Behavioral and Brain Sciences (1991). The omission is regrettable, it was unintentional, and I missed that article just as it seems to have escaped the attention of MEDLINE. Regardless, the article by Dr. Gray and colleagues also tried to address how a neurobiological lesion might lead to symptoms by means of the disruption of a core psychological process. However, there are major differences. The focus of their claim is a putative neuroanatomical lesion (of the hippocampus or accumbens), not the clinical picture or phenomenology. The core psychological lesion in their model is a "failure…to integrate stored memories…with ongoing motor programs," as opposed to concepts of reward/salience, as in my article. Apart from the fact that antipsychotics are seen as dopamine blockers, little attention is paid to the nature and phenomenology of antipsychotic response and less still is said about the process of symptom resolution. As for the critique that I unfairly dismissed latent inhibition as a model of attentional abnormalities, some of the authors of the article by Dr. Gray et al. also see it as a model of attentional deficits (1), and others question whether it models attentional deficits at all (2, 3). Furthermore, the single largest clinical study of latent inhibition failed to find evidence for a disruption of latent inhibition or for the effects of treatment on latent inhibition (4). Nonetheless, I agree with their final point: that this discussion belonged in the original article, not here as an afterthought.