FGF23 is crucial for phosphate homeostasis including physiological and pathophysiological conditions such as X-linked hypophosphatemic rickets and it seems that FGF23 is probably the most important regulator of serum phosphate and calcitriol (1,25(OH)2D3) levels in addition to parathyroid hormone (PTH) produced by the parathyroid gland (9-13). FGF23 is produced by osteocytes and osteoblasts, secreted in response to phosphate, and 1,25(OH)2D3, binds to the FGF receptor (FGFR)/Klotho complex, and acts as a phosphaturic hormone by reducing the expression of both sodium dependent phosphate cotransporters, namely NaPi2a and NaPi2c in renal proximal tubule cells (14). There is some evidence of PTH induced expression and secretion of FGF23 and on the other hand FGF23 decreases 1,25(OH)2D3 production and thus stimulates PTH production. In chronic kidney disease (CKD) patients, FGF23 is involved in CKD-related mineral and bone disorder (CKD-MBD) and has been shown to be an independent and probably more critical cardiovascular risk factor than phosphate (14).