Iron deficiency, hyperphosphatemia, and inflammation contribute to FGF23 production during CKD.1,8,9 Whether the effects of Lcn2 deletion on FGF23 production in CKD are partially mediated by the increase in circulating iron or decrease in circulating phosphate that we observed in CPD mice requires further study, but the lack of effects of LCN2 deletion on FGF23 regulation in diet-induced iron deficiency strongly suggests an iron independent effect. This evidence concerns the gene FGF23 and chronic kidney disease.