In Hyp mice, the osteocytic expression of Fgf1, Fgf2, Fgfr1–3, and Egr-1, which is a target gene of activated FGFR signaling, was found to be markedly up-regulated (8), and the osteocyte-specific deletion of Fgfr1 partially restored the overproduction of FGF23 and attenuated hypophosphatemia and mineralization defects (29). Here, FGFR1 is linked to hypophosphatemia.