Several animal models with excess FGF-23 activity as a result of in vivo forced overexpression exhibit hypophosphatemia and increased P excretion of 1,25-dihydroxyvitamin D [1,25(OH)2D] [5–8], and Fgf23 knockout (KO) mice are characterized by increased renal P reabsorption and an elevated serum 1,25(OH)2D concentration [9, 10]. This evidence concerns the gene FGF23 and hypophosphatemia.