Reductions in GABAergic neuron markers (eg, GAD67, parvalbumin, and somatostatin) within the prefrontal cortex are one of the most replicated post-mortem findings in schizophrenia.15–18 These findings appear to reflect altered functioning, rather than loss of subpopulations of these neurons15,18 and have been hypothesized to have a developmental basis.19–21 Disturbances in cholinergic neuron function have also been postulated to play a role in the pathophysiology of schizophrenia,22–24 with dysfunction in either system plausibly contributing to the diverse symptomatology of the disorder. The gene discussed is GAD1; the disease is schizophrenia.