The cellular mechanism of the early stage of DCM involves elevated levels of free fatty acids, changes in Ca2+ homeostasis, reduced expressions of GLUT-1 and GLUT-4, while the middle stage of DCM involves insulin resistance, apoptosis, necrosis, fibrosis, mild cardiovascular autonomic neuropathy, formation of advanced glycation end products, elevated levels of the renin–angiotensin–aldosterone system (RAAS), and TGF-β1, with a decrease in IGF-1 (Chavali et al., 2013). This evidence concerns the gene TGFB1 and familial dilated cardiomyopathy.