Understanding the physiologic regulation and interaction of FGF23 and vitamin D helped in determining the pathomechanisms of renal phosphate-wasting diseases, including XLH, autosomal dominant hypophosphatemic rickets, or tumor-induced osteomalacia (TIO); all three of these diseases are characterized by extremely high circulating levels of bioactive (intact) FGF23 (48, 49). This evidence concerns the gene FGF23 and X-linked hypophosphatemia.