In hereditary hypophosphatemic disorders, such as X-linked hypophosphatemia (XLH) and autosomal recessive hypophosphatemic rickets (ARHR), the primary increase in circulating FGF23 levels leads to renal Pi wasting, causing hypophosphatemia and secondary alterations in mineral and bone metabolism, such as hyperparathyroidism, rickets, and osteomalacia (3–7). This evidence concerns the gene FGF23 and hypophosphatemia.