Our studies showed that A-MG promotes AKT phosphorylation, which inhibits FOXO1 activation and sustains glucose utilization at the expense of β-oxidation of FAs to reduce oxidative stress-related apoptosis of cardiomyocytes under HG/F conditions in vitro and DCM modeling in vivo. This evidence concerns the gene FOXO1 and familial dilated cardiomyopathy.