The main function of FGF23 seems to be regulation of phosphate concentration in plasma. FGF23 is secreted by osteocytes in response to elevated calcitriol. FGF23 acts on the kidneys, where it decreases the expression of NPT2, a sodium-phosphate cotransporter in the proximal tubule. Thus, FGF23 decreases the reabsorption of calcium and increases excretion of phosphate. 
Loss of FGF23 activity is thought to lead to increased phosphate levels and the clinical syndrome of familial tumor calcinosis. This gene was identified by its mutations associated with autosomal dominant hypophosphatemic rickets. Mice lacking either FGF23 or the klotho enzyme display premature aging due to hyperphosphatemia.
Prior to its discovery in 2000, it was hypothesized that a protein existed which performed the functions subsequently shown for FGF23. This putative protein was known as phosphatonin. Several types of effects were described including impairment of sodium dependent phosphate transport in both intestinal and renal brush border membrane vesicles, inhibition of production of calcitriol, stimulation of breakdown of calcitriol, and inhibition of production/secretion of parathyroid hormone.
^Yamashita T, Yoshioka M, Itoh N (October 2000). "Identification of a novel fibroblast growth factor, FGF-23, preferentially expressed in the ventrolateral thalamic nucleus of the brain". Biochemical and Biophysical Research Communications. 277 (2): 494–8. doi:10.1006/bbrc.2000.3696. PMID11032749.
^ abPerwad F, Zhang MY, Tenenhouse HS, Portale AA (November 2007). "Fibroblast growth factor 23 impairs phosphorus and vitamin D metabolism in vivo and suppresses 25-hydroxyvitamin D-1alpha-hydroxylase expression in vitro". American Journal of Physiology. Renal Physiology. 293 (5): F1577-83. doi:10.1152/ajprenal.00463.2006. PMID17699549.
Quarles LD (July 2003). "FGF23, PHEX, and MEPE regulation of phosphate homeostasis and skeletal mineralization". American Journal of Physiology. Endocrinology and Metabolism. 285 (1): E1-9. doi:10.1152/ajpendo.00016.2003. PMID12791601.
Bowe AE, Finnegan R, Jan de Beur SM, Cho J, Levine MA, Kumar R, Schiavi SC (June 2001). "FGF-23 inhibits renal tubular phosphate transport and is a PHEX substrate". Biochemical and Biophysical Research Communications. 284 (4): 977–81. doi:10.1006/bbrc.2001.5084. PMID11409890.
White KE, Carn G, Lorenz-Depiereux B, Benet-Pages A, Strom TM, Econs MJ (December 2001). "Autosomal-dominant hypophosphatemic rickets (ADHR) mutations stabilize FGF-23". Kidney International. 60 (6): 2079–86. doi:10.1046/j.1523-1755.2001.00064.x. PMID11737582.
Kruse K, Woelfel D, Strom TM, Storm TM (2002). "Loss of renal phosphate wasting in a child with autosomal dominant hypophosphatemic rickets caused by a FGF23 mutation". Hormone Research. 55 (6): 305–8. doi:10.1159/000050018. PMID11805436. S2CID46748089.