Hypocalcemia occurred after weaning in the 1α(OH)ase−/− mice with deficient 1,25(OH)2D production but intact Vdr, and treatment with exogenous 1,25(OH)2D3 normalized serum calcium.(9) In contrast, in the Vdr−/− mice with elevated endogenous levels of 1,25(OH)2D, deficiency of Vdr, resulted in hypocalcemia which was not corrected by exogenous 1,25(OH)2D3 treatment, indicating that both 1,25(OH)2D and the VDR are necessary for optimal intestinal absorption of calcium. Here, VDR is linked to Hypocalcemia.