While Gad1 is mainly responsible for the GABA synthesis in the brain.32 The VGAT biological function was mainly involved in GABA uptake into synaptic vesicles in the presynaptic vesicular membranes.33 Furthermore, GABA transporter proteins can either be expressed on neurons or glial cells, which can mediate uptake of GABA from the synaptic cleft.34 The consistent results from our study suggested that GABA‐associated mRNAs and proteins expression were decreased in CUMS‐induced depression mice. The gene discussed is SLC32A1; the disease is depressive disorder.