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]. The gene discussed is EPO; the disease is anemia (phenotype).