At the mechanistic level, intracellular iron sequestration is mediated by the hepcidin‐induced internalization and degradation of ferroportin, the only iron exporter identified to date.3 The hepcidin‐ferroportin axis is therefore a promising therapeutic target for treating many iron disorders, including haemochromatosis, β‐thalassaemia, anaemia of chronic disease and iron‐refractory iron deficiency anaemia.9 This evidence concerns the gene HAMP and hereditary hemochromatosis.