Deficiency of klotho also appears to reduce osteoblastic population andinterfere with bone mineralization.7 Together, the FGF receptor–Klotho complex inhibits sodium-dependent phosphateuptake and 1α-hydroxylase activity in the proximal tubule of the kidney, leading tohypophosphatemia and inappropriate low 1,25(OH)2D.8 In contrast, a deficiency of either FGF23 or klotho results in the oppositephenotype of hyperphosphatemia and elevated production of 1, 25(OH)2D,further confirming the role of FGF23 in regulation of serum phosphate and1,25(OH)2D levels. This evidence concerns the gene KL and hyperphosphatemia.