Suppression of hepcidin can be physiologic, facilitating iron absorption and making recycled iron available for cells in conditions of ID or stress erythropoiesis, but it can also be harmful in patients with ineffective erythropoiesis due to genetic conditions such as thalassemia or congenital dyserythropoietic anemia, or due to genetic disruption of the hepcidin regulatory pathways in hereditary hemochromatosis. The gene discussed is HAMP; the disease is thalassemia.