While some evidences link it to cardiac hypertrophy through intracellular pathways involving cytoplasmic Ca2+, RAS proteins, mitogen-activated protein kinases (MAPK) and inositol 3,4,5-triphosphate (IP3) generated by phospholipase C [15], other findings associate GPR91 to the induction of apoptosis in cardiomyocytes through the activation of protein kinase A (PKA) [16]. The gene discussed is SUCNR1; the disease is cardiac hypertrophy.