Recent findings underscore the critical role of ferroptosis in the development of diabetic cardiomyopathy.[97–99] Iron overload can exacerbate cardiovascular complications in diabetic patients through the Fenton reaction.[100] Wang et al[101] found that advanced glycation end-products induce ferroptosis by increasing lipid peroxide levels and decreasing the expression of ferritin and recombinant Solute Carrier Family 7 Member 11, resulting in iron overload and GSH deficiency, which ultimately leads to DCM in T2D mice. The gene discussed is SLC17A1; the disease is familial dilated cardiomyopathy.