It is well known that Ca2+ played a detrimental role in heart failure and myocardial ischemia/reperfusion, and Ca2+ overload activated the complex matrix chaperone procyclin D (CypD), which regulated the VDAC1, Grp75, and IP3R1 complex and thus caused damage to cardiomyocytes, whereas inhibition of the CypD, VDAC1, Grp75, and IP3R1 complex could protect cardiomyocytes49. The gene discussed is ITPR1; the disease is heart failure.