Postmortem studies report reduced mRNA level and expression of the GABA synthesizing enzyme, 67 kDa isoform of glutamic acid decarboxylase (GAD67), and GAT1, as well as an apparent upregulation of postsynaptic GABAA receptors (GABAARs) in the prefrontal cortex of human subjects with schizophrenia [3], suggesting a mechanism for abnormal GABAergic neurotransmission in schizophrenia. The gene discussed is GAD1; the disease is schizophrenia.