Studies have shown that cardiac‐specific FPN1 knockout mice exhibit an imbalance in myocardial iron metabolism and cardiac insufficiency, whereas cardiomyocyte‐specific knockout of hepcidin leads to the deregulation of cardiac FPN1 and lethal iron deficiency due to increased iron efflux, suggesting an important role for the hepcidin‐FPN1 axis in the regulation of iron cardiomyocyte homeostasis.22, 23, 24. This evidence concerns the gene HAMP and nutritional disorder.