Although hepcidin suppression has been recognized as major mechanisms of chronic iron accumulation in most hereditary iron overload diseases such as hemochromatosis (17), hepcidin is seemingly paradoxically and profoundly suppressed in hemolytic diseases such as thalassemia (18) or chronic liver diseases (19) in the presence of iron excess, for example, released from an increased red blood cell turnover (19, 20). This evidence concerns the gene HAMP and thalassemia.