Some of these cellular and biochemical changes, including reduction of GABA transmission and GABA‐synthesizing enzyme 67 (GAD67) protein levels, as well as GABAA/B receptor deficits, are observed in animal models of MDD (Luscher et al, 2011; Banasr et al, 2017; Jacobson et al, 2018; Duman et al, 2019), leading to the hypothesis of disrupted structural and functional integrity of prefrontal GABAergic networks as a pathophysiological basis of MDD. Here, GAD1 is linked to major depressive disorder.