Based on those observations, they proposed for the first time the existence of a basic abnormality in the retention of iron in macrophages and probably from intestinal mucosal cells [38], a mechanism that is presently well established with the demonstration that hepcidin, which is functionally defective in hemochromatosis, regulates cellular iron efflux by binding to ferroportin and inducing its internalization [3]. Here, SLC40A1 is linked to hemochromatosis.