Cancer patients have been characterized by decreased iron availability in mitochondria, and iron supplementation was sufficient to preserve muscle function.[45] As reported, muscles from old mice had increased iron levels, which were associated with increased susceptibility to ischemia‐reperfusion injury and impaired muscle regeneration.[46] Herein, our data demonstrated that Huwe1 deficiency in the skeletal muscle leads to iron overload through downregulating Fpn, which exports iron from cells to plasma. The gene discussed is SLC40A1; the disease is cancer.