The presence of iron overload in FD patients with loss-of-function mutations and hence reduced duodenal iron absorption indicates the existence of differences of FPN production and activity between enterocytes and macrophages, which could be related to FPN transcriptional and translational regulation, assistance in iron export by different oxidases (membrane-bound hephaestin for enterocytes and circulating ceruloplasmin for macrophages) or to the tenfold difference in iron trafficking between these two cell types [43]. The gene discussed is SLC40A1; the disease is Tangier disease.