Hepcidin gene expression is controlled by many factors [5], obviously including body iron levels; iron-mediated regulation largely depends on the BMP/SMAD pathway whose activation requires genes like HFE, hemojuvelin, and transferrin receptor 2 (TfR2) that are inactivated in various forms of hereditary hemochromatosis [6]. This evidence concerns the gene TFR2 and hereditary hemochromatosis.