Also, we must consider the complexity of mechanisms of sepsis-related anemia and interaction of relevant parameters: the non-availability of iron for erythropoiesis despite high iron reserves in tissue; a blunted erythropoietic effect of EPO by pro-inflammatory cytokines; suppression of hepcidin by erythroferrone (thus facilitating iron delivery during stress erythropoiesis); erythroferrone production induced by EPO; regulated systemic uptake and recycling of iron by hepcidin through inhibition of the hepcidin–ferroportin interaction [2, 8, 9, 17, 34, 35, 38, 39]. This evidence concerns the gene EPO and Sepsis.