During the transition from a stressful state to depression, increased GPR158 expression induced by long-lasting stress resulted in RGS7 being directed to the plasma membrane, and this GPR158–RGS7 complex modulated the function of the GTPase accelerating protein (GAP) complex to regulate adenylate cyclase (AC) and cAMP production in the mPFC [19,24]. The gene discussed is GPR158; the disease is depressive symptom measurement.