GALNT3 mutations lead to inactivated cleavage of FGF23 and dysregulation of phosphate homeostasis resulting in familial tumoral calcinosis (FTC), characterized by hyperphosphatemia, altered bone density, and the development of subcutaneous calcified tumors; whereas under normal conditions, GALNT3 mediated FGF23 glycosylation protects FGF23 from protease cleavage [33,34]. Here, FGF23 is linked to hyperphosphatemia.