For example, although circulating growth differentiation factor 15 (GDF15) increases in patients with some congenital and acquired anemias and inversely correlates with hepcidin (Tanno et al., 2007), levels of GDF15 and hepcidin correlate poorly in phlebotomized mice (Casanovas et al., 2013) and in MDS patients (Santini et al., 2011), suggesting that mechanisms of hepcidin suppression by erythropoiesis may be disease specific. This evidence concerns the gene HAMP and myelodysplastic syndrome.