Evidence supporting the role of GABA in schizophrenia development includes the deficiency of GABA synthesis resulting from reduced transcription of the 67-kDa isoform of glutamic acid decarboxylase (GAD67) within parvalbumin-immunoreactive cortical neurons and the reduction in the subpopulation of GABAergic interneurons positive for parvalbumin and the β2 subunit of the GABAA receptor (GABAAR) in animal studies and in the post-mortem brains of schizophrenia patients18, 19, 20, 21, 22. This evidence concerns the gene PVALB and schizophrenia.