During clinical anemia, FGF23 can be markedly elevated37,38 and it has been shown that FGF23 can be suppressed in ADHR patients receiving oral iron, effectively curing the ADHR renal phosphate wasting and metabolic bone disease.19 To test the concept that improved iron utilization directly controls circulating Fgf23, and that Phd2 is required for this process, an in vitro model of iron deficiency was employed. This evidence concerns the gene EGLN1 and anemia.