These cellular events are due to hyperinsulinemia and increased free fatty acid accumulation and oxidation in insulin-resistant adipocytes and cardiomyocytes, which contribute to the development and progression of DCM, and could account for the diastolic dysfunction in 40–75% of diabetic patients without coronary artery disease (Shivalkar et al., 2006; Brooks et al., 2008; Fukuda et al., 2010; Kuramoto et al., 2014; Jaishy et al., 2015). The gene discussed is INS; the disease is hyperinsulinism.