The human erythron is responsible for oxygen transport and includes the erythroid marrow, circulating red cells, the réticulo-endothelial system and the erythropoietin producing cells in the kidney. These renal cells have a mechanism for oxygen sensing. In normoxia oxygen activates the PH factor which hydroxylate a subunit of the transcription factor HIF. In hypoxia this subunit HIFα together with the subunit HIFβ activate EPO gene. Increased EPO binds to the receptor on erythroid progenitors and leads to increased red cells production as an appropriate response to hypoxia.Alterations in the oxygen sensing pathway and abnormalities of the EPO signaling pathway lead to primary and secondary erythrocytosis.Immature erythroid cells are the major consumers of iron in the body. Elevated erythropoesis increases intestinal iron absorption and stocked iron mobilization. Considering its potential toxicity and low bioavailability, iron metabolism is a tightly regulated process in humans. Control mechanisms maintain iron homeostasis by coordinately regulating iron absorption, iron recycling and mobilization of stored iron.Dietary iron absorption is locally regulated by HIF and IRPs in enterocytes and systematically by hepatic hepcidin, the central iron regulatory hormone. Hepcidin not only controls the rate of iron absorption but also determines iron mobilization from stocks through modulating ferroportin protein.