 This leads to maximal iron absorption from ingested foods and iron overload in the tissues.However, "HFE" is only part of the story, since many patients with mutated "HFE" do not manifest clinical iron overload, and some patients with iron overload have a normal "HFE" genotype.A possible explanation is the fact that "HFE" normally plays a role in the production of hepcidin in the liver, a function that is impaired in "HFE" mutations.