Studies demonstrate that activating G protein-coupled estrogen receptor (GPER) ameliorates cardiac structural abnormalities in type 2 diabetes (T2D) rat models through dual molecular mechanisms (108): concomitant downregulation of ERS markers (chaperone Bip, apoptosis-related caspase-12, and pro-apoptotic Bax) and reversal of suppressed SERCA2α and anti-apoptotic Bcl-2 expression. The gene discussed is CASP12; the disease is type 2 diabetes mellitus.