Our current, previous and number of recent studies using different hemochromatosis mouse models show that mice lacking Hfe,31 transferrin receptor 2,56 hemojuvelin, and hepatocyte-specific Alk2 and Alk3, do not develop bone loss,57 contrary to potential site-specific bone deficits observed in hepcidin-resistant ferroportin FpnC326S mutant mice,58 and in hepcidin-deficient mice59,60; notably, the latter 2 models present the highest iron loading among all hemochromatosis models. The gene discussed is HAMP; the disease is hemochromatosis type 1.