It was recently shown clinically that FGF23 mediated the risks of heart failure and mortality associated with iron deficiency in CKD patients.29 Herein, we used an in vitro model of osteocyte iron deficiency with iron repletion via holo-transferrin demonstrated direct actions on the osteocyte to regulate Fgf23 expression, and further, that Phd2 is necessary for iron-mediated suppression of Fgf23. The gene discussed is EGLN1; the disease is chronic kidney disease.