SLC32A1 and schizophrenia: In schizophrenia and bipolar patients, the number of PV interneurons and the expression level of molecular components of GABAergic synapses, such as glutamic acid decarboxylase 67 (GAD67) and vesicular gamma-amino-butyric acid (GABA) transporter (VGAT), are found decreased in post-mortem brains leading to the ‘GABA hypofunction hypothesis' as a potential etiology.1, 11, 12, 13, 14, 15, 16 Yet, the molecular understanding of how such a detrimental loss of the GABAergic system might lead to corrupted cortical networks manifesting in disease, remains poorly explored.