Two of these mouse models (Pvalb/Gad1-silencing mice and PV-Cre; GAD67+/flox mice) showed altered prepulse inhibition and responsiveness to NMDA receptor antagonists and a partially schizophrenia-like phenotype but no apparent working memory impairment (Brown et al., 2015; Fujihara et al., 2015a). The gene discussed is GAD1; the disease is schizophrenia.