Cancer cells with aberrant GAD1 expression had altered glutamine metabolism in non-neural tissues to synthesize the important neurotransmitter, GABA. GABA activated the GABAB receptor to depress GSK-3β activity, leading to enhanced β-catenin signaling, which ultimately caused to not only stimulation of tumor cell proliferation, but also inhibition of intratumoral infiltration of CD8 + T cells [48]. Here, GSK3B is linked to neoplasm.