Lin et al. reduced DCM in type 2 diabetic mouse model by activating integrin αVβ5/AKT signaling and reducing oxidative & nitrosative stress in db/db mice and inhibited cardiomyocyte apoptosis, myocardial fibrosis, and cardiac hypertrophy in db/db mice by exogenous irisin supplementation, thereby reducing diastolic dysfunction and cardiac [32]. This evidence concerns the gene AKT1 and familial dilated cardiomyopathy.