Specifically, patients with HCC are characterized by an abnormal iron uptake [7], an excessive accumulation of hepatic iron [5], a prevalence of mutations in the hemochromatosis (HFE) gene [8], one of the main mediators of iron metabolism, and a pronounced suppression in the expression of hepcidin (HAMP) [9], the central regulator of iron homeostasis in mammals [10]. The gene discussed is HAMP; the disease is hemochromatosis type 1.