It has been shown that low FGF23 activity due to mutations in GALNT3, FGF23, and Klotho leads to familial hyperphosphatemic tumoral calcinosis, which is characterized by enhanced renal tubular phosphate reabsorption and high serum 1,25(OH)2D level in hyperphosphatemia[20-22]. Here, FGF23 is linked to hyperphosphatemia.