Hepcidin regulation by erythropoiesis and its effects on iron efflux from cells involved in iron metabolism. Hepcidin plays a central role in the maintenance of iron homeostasis and regulation of plasma iron concentrations by controlling ferroportin concentrations on iron-exporting cells, including duodenal enterocytes, recycling macrophages of the spleen and liver, and hepatocytes (involved in iron storage). The bone marrow has the highest iron requirements for hemoglobin synthesis, and thus, increased erythropoietic activity suppresses hepcidin production. Several potential candidate erythroid regulators of hepcidin (eg, GDF15 and TWSG1) in β-thalassemia have been reported. Recently, a non–disease-specific mechanism has been proposed (eg, ERFE). EPO, erythropoietin; Fe, iron; TWSG1, twisted gastrulation 1.