My colleagues and I made a similar proposal in 1991, in greater anatomical and physiological detail and with similar claims for bridging the neural basis of psychosis to its symptoms. This article (2) appeared in a widely cited journal, Behavioral and Brain Sciences, whose exacting refereeing process ensured that we made proper reference to our own forerunners. It did not pass unnoticed. Over the period 1991–1999, it was the eighth most frequently cited article in schizophrenia research (http://esi-topics.com/schizophrenia/papers/a1.html). Its authors, including David Hemsley, Joram Feldon, and myself, have developed, applied, and reviewed these initial ideas in further publications (e.g., references 3–6). We also proposed a number of empirical tests of our hypotheses. One, a disruption of latent inhibition by augmented dopaminergic transmission in the nucleus accumbens, investigates just that process of "aberrant assignment of salience to external objects"—or "spurious novelty" (7)—that is central to Dr. Kapur’s model. One might have expected him, therefore, to seek support in, or at least discuss, the abundant data concerning disrupted latent inhibition gathered since 1991 in numerous experiments with both animal and human subjects (4–7). Instead, in a lone mention, he dismisses latent inhibition as a "model of attentional habituation" (p. 18), a simplistic account that was considered and dismissed in our 1991 authors’ response to multiple peer review in Behavioral and Brain Sciences(2). We stressed then, just as Dr. Kapur did, the critical role of contextual dependence of salience attribution, applying this concept in particular to latent inhibition and its disruption.