HIF-2 transcriptionally regulates the expression of key genes involved in iron transport. Under conditions of iron deficiency, hypoxia, or increased erythropoietic drive, HIF-2 is stabilized in the duodenal enterocyte and transcriptionally upregulates the expression of DMT1 + iron responsive element (IRE), DCYTB, and FPN. This leads to increased expression of DMT1 and DCYTB at the apical brush border membrane and FPN at the basal membrane.^29,52,53,58  The direct binding of HIF-2 to consensus HRE elements in the regulatory regions of the promoters has been shown for DCYTB and DMT1. At the systemic level, hepatic hepcidin is repressed, preventing its inhibitory action on duodenal iron absorption.