Different mechanisms in myocardial iron uptake and metabolism have been proposed for this finding.54 Differences in hepcidin levels may also play a role, being most profoundly suppressed in NTDT, less so in TM (regular transfusion suppresses ineffective erythropoiesis and erythroferrone, which inhibits hepcidin production),55,56 normal or elevated in sickle cell disease57,58 and reported as elevated in MDS in one study.57 Elevated hepcidin inhibits iron release from the reticuloendothelial system, reducing iron accumulation in parenchymal cells. Here, HAMP is linked to myelodysplastic syndrome.