Previous studies have demonstrated that the levels of the iron transport proteins transferrin receptor 1 (TFR1, cell membrane) and mitoferrin 1 (MFRN1, mitochondrial membrane) are increased in the cardiomyocytes of diabetic mice, which is the direct cause of iron overload in the cytoplasm and mitochondria.[39] Excessive levels of iron ions further exacerbate oxidative stress, and the inhibition of the GSH/GPX4 pathway induces ferroptosis in cardiomyocytes, which is another mechanism underlying cardiac damage in DCM.[39]. The gene discussed is TFRC; the disease is familial dilated cardiomyopathy.