Blood transfusions modify hepcidin production by altering all three factors responsible for the clinical manifestations of TI described above namely: (i) by correcting anaemia, transfusion therapy will suppress ineffective erythropoiesis and the associated increase in GDF15; (ii) by correcting anaemia, blood transfusions will prevent the hypoxia responsible for increased HIF production and hypoxia-associated suppression of hepcidin; and (iii) increased body iron and transferrin saturation will stimulate hepcidin production. The gene discussed is GDF15; the disease is anemia (phenotype).