This iron overload is due to ineffective erythropoiesis, similar to what occurs in congenital dyserythropoietic anemias, thalassemia, and anemias with decreased hepcidin and increased intestinal iron absorption [51,53] In most patients with congenital sideroblastic anemias and with MDS-RS, the study of iron parameters reveals an increase in serum iron, ferritin, and transferrin saturation at diagnosis, even before the patient has required transfusion support [54]. The gene discussed is HAMP; the disease is thalassemia.