Efforts to treat XLH medically have focused primarily on modifying the influence of FGF23 on renal phosphate handling and 1,25-dihydroxyvitamin D production, or administration of conventional therapy, neither of which are likely to address aspects of the disease that are not mediated by FGF23, hypophosphatemia, or impaired vitamin D activation. This evidence concerns the gene FGF23 and hypophosphatemia.