Deletion of intestinal Hif2α or pharmacological blockade of Hif2α using a clinically relevant inhibitor PT2385 successfully reduced iron accumulation in a mouse model of hepcidin‐deficient hemochromatosis.[23, 45] Besides, intestine‐specific disruption of Hif2α[46, 47] or dietary iron restriction[48] or use of the oral Fpn inhibitor vamifeport[49, 50, 51] has been reported to improve iron‐overloaded anemias, such as sickle cell disease and β‐thalassemia in mice. This evidence concerns the gene SLC40A1 and sickle cell disease.