Interestingly, the abundance of IRP2 is controlled in an iron-dependent manner by iron-sensing F-box and leucine-rich repeat protein 5 (FBXL5), ablation of which in an FBXL5-deficient mouse model leads to IRP2 overactivity-dependent iron overload, promoting oxidative stress, lipid peroxidation, tissue damage, inflammation and compensatory proliferation of hepatocytes, resulting in the promotion of HCC development in the case of exposure to diethylnitrosamine in mice. The gene discussed is IREB2; the disease is hepatocellular carcinoma.