The genetic basis for XLH is the loss of function of the PHEX gene, located in chromosome Xp22; this loss results in an elevation of the serum levels of fibroblast growth factor 23 (FGF23), and impaired renal production of 1,25-dihydroxyvitamin D (1,25-(OH)2D). This evidence concerns the gene FGF23 and X-linked dominant hypophosphatemic rickets.