Hepcidin coordinates iron supply for erythropoiesis. Hepcidin controls major iron flows into plasma by causing degradation of its receptor ferroportin. After erythropoietic stimulation, erythroid precursors secrete 1 or more mediators (erythroid factors) that suppress hepcidin production in the liver, resulting in increased iron supply to the bone marrow. ERFE has been proposed to mediate hepcidin suppression in both physiological (eg, after hemorrhage) and pathological conditions (eg, ineffective erythropoiesis), whereas GDF15 and TWSG1 may only play a role in iron-loading anemias. Other erythroid regulators may exist but have yet to be identified.