Hyperphosphatemia, iron deficiency/anemia, and inflammation are potent stimuli of bone FGF23 production during CKD progression.2,8 We tested whether Lcn2 deletion would alter FGF23 regulation by phosphate, iron, or inflammatory stimuli induced by dietary Pi loading, iron restriction, and acute IL1β injections, respectively. The gene discussed is LCN2; the disease is chronic kidney disease.