Several abnormalities in GABA neurotransmission have been reported in patients with schizophrenia and TRS, such as morphological alterations in cortical and hippocampal GABA interneurons [108], reductions in cerebrospinal fluid (CSF) GABA levels in first-episode psychosis (FEP) [111], decreased glutamic acid decarboxylase (GAD67) levels in the dorsolateral PFC (DLPFC) [112,113], reduction in GABAB receptors expression in the post-mortem PFC and hippocampus [114,115], and genetic polymorphisms of GAD67, GABBR1, and GABBR2 genes, which encode for the GABAB receptor [116]. This evidence concerns the gene GABBR2 and schizophrenia.