The development of DCM involves a variety of mechanisms of decisive molecular, cellular and interstitial changes, including myocardial energy substrate imbalance, glucose and lipid toxicity, insulin signal changes, mitochondrial defects, endoplasmic reticulum (ER) stress, intracellular calcium processing disorder, oxidative stress, endothelial dysfunction, advanced glycation end products (AGEs) deposition, and maladaptive immune response. The gene discussed is INS; the disease is familial dilated cardiomyopathy.