In the cortex of subjects with schizophrenia, inhibitory neurotransmission mediated by γ-aminobutyric acid (GABA) appears to be altered [2], as indicated by lower levels of the mRNAs encoding the 67 kilodalton isoform of glutamic acid decarboxylase (GAD67) [3], the enzyme principally responsible for GABA synthesis, and the GABA membrane transporter 1 (GAT1) [4], [5], [6], [7], [8], which mediates the reuptake of synaptically released GABA. The gene discussed is GAD1; the disease is schizophrenia.