This study demonstrated the link between iron and oxygen sensing pathways in osteocytes regulating FGF23, and is in line with previous findings of HIF activation of FGF23 transcription.3,4,16,17 Consistent with the pre-clinical ADHR mouse findings, patients with ADHR have elevated intact, bioactive FGF23.18 These patients can be cured with iron treatment to suppress FGF23,19 however, the mechanisms controlling FGF23 during hypoxia/anemia, as well as the direct actions of iron therapy on osteocytes are unknown. The gene discussed is FGF23; the disease is autosomal dominant hypophosphatemic rickets.