The results suggest that expanded but ineffective erythropoietic activity in these patients leads to inappropriately low hepcidin levels in MDS-RARS patients with an SF3B1 mutation, leading ultimately to excess release of iron from the RES and parenchymal iron loading (Ambaglio et al., 2013). This evidence concerns the gene SF3B1 and myelodysplastic syndrome with ring sideroblasts.