A critical manifestation arising in CKD is anemia due to lack of EPO production and/or EPO resistance, inflammation, or bleeding.24 Delivery of a novel class of oxygen mimetics, hypoxia-inducible factor-prolyl hydroxylase inhibitors (HIF-PHI) stabilize HIFs via PHD inhibition which increase endogenous EPO, or recombinant EPO itself, can cure the anemia of CKD.25,26 With resolving the IDA of a CKD mouse model, it was shown that FGF23 levels are reduced, supporting that FGF23 is strongly stimulated by hypoxia/anemia in this disease. The gene discussed is FGF23; the disease is chronic kidney disease.