Imbalance of calcium homeostasis in the cardiomyocytes not only directly interferes myocardial contraction and relaxation through calcium/calmodulin-dependent proteins but also exacerbates the heart failure process by interacting with other pathophysiological factors such as the β-adrenergic signaling pathway and renin-angiotensin-aldosterone system (RAAS) [27–30]. This evidence concerns the gene REN and heart failure.