We and others have investigated the brain iron phenotype of mice with disruption of the Hfe gene (Hfe−/−) or the transferrin receptor 2 gene (Tfr2mut), the iron regulatory genes causatively associated with hemochromatosis.11, 12, 13 However, although these models display chronic systemic iron loading, brain iron content remained unchanged at all ages investigated,11, 12 as also reported for a related Hfe H67D mutation ‘knock-in' mouse model.14 The gene discussed is HFE; the disease is hemochromatosis.