In contrast to the hypophosphatemia owing to an FGF-23-mediated increase in urinary phosphate excretion observed in patients lacking functional DMP1, GALNT3 and FGF23 mutations result in hyperphosphatemia owing to inappropriately low urinary phosphate excretion and low intact FGF-23 levels leading to the development of tumoral calcinosis. The gene discussed is FGF23; the disease is hyperphosphatemia.