In spite of the etiopathogenic definition of HC as an hepcidin insufficiency, its observed correlation with iron reaccumulation could be expected based on the evidence from animal models showing that the response to chronic iron challenge in Hfe deficient mice is only partially blunted.8 An alternative hypothesis to explain the correlation between ferritin and hepcidin is that HC patients could be particularly sensitive to signs of iron deficiency, with concomitant hepcidin downregulation in response to the erythroid stimulation induced by phlebotomies, in spite of normal iron parameters. The gene discussed is HAMP; the disease is nutritional disorder.