Hepcidin expression in the liver of FECH-deficient animals was not suppressed, although these animals exhibited severe anemia, suggesting that erythropoiesis was not restricted by an absolute iron deficiency but likely limited by iron compartmentalization (i.e., functional iron deficiency), and/or the presence of strong up-regulators of hepcidin in this experimental setting. The gene discussed is FECH; the disease is Iron deficiency anemia.