FGF23 and X-linked dominant hypophosphatemic rickets: A study of Hyp mice, an animal model of XLHR caused by mutations in the PHEX gene [13], showed that FGF23 acted downstream of PHEX and that a PHEX mutation directly enhanced the secretion of FGF23 by osteoblasts, leading to reduced renal phosphate resorption and disrupted bone phenotypes [14].