For the mechanisms of DCM, impaired insulin metabolic signaling, hyperglycemia-induced abnormal AGE/receptor for advanced glycation end product (RAGE) signaling, mitochondrial dysfunction, increased fatty acid utilization, endoplasmic reticulum stress, and impaired calcium handling, in conjunction with coronary endothelial dysfunction, are considered pathogenic causes in type 2 diabetes- (T2DM-) induced DCM [5, 10, 11]. This evidence concerns the gene AGER and type 2 diabetes mellitus.