Due to the lacking suppressive effect of Fgf23 on renal 1α-hydroxylase activity, Kl−/− and Fgf23−/− mice produce excessive amounts of 1,25(OH)2D, and die early from the sequelae of hypervitaminosis D, hypercalcemia and hyperphosphatemia. Here, FGF23 is linked to hypercalcemia disease.