Pharmacological inhibition of HIF-PHs increases EPO and DMT1 (ferrous ion membrane transport protein 1)/Nramp2 (NRAMP metal ion transporter 2) in the intestinal epithelium and decreases hepcidin production in the liver, thereby improving iron metabolism in vivo and potentially leading to efficient treatment of not only CDK-induced anemia but also anemia associated with chronic diseases [11,21,22,23]. This evidence concerns the gene SLC11A2 and anemia (phenotype).