The genetics and the clinical manifestations of hemochromatosis are very complex (106), but iron overload is seen irrespective of whether the genetic lesion refers to HFE or β2M. Nevertheless, there are important biochemical differences, since β2M-deficient mice have higher hepcidin levels which correlate inversely with the severity of hepatic iron overload (88). This evidence concerns the gene B2M and hemochromatosis type 1.