Global VDR-/- mice, as well as mutants with a non-functioning VDR (VDRΔ/Δ), are characterized by an intestinal calcium absorption defect and develop severe secondary hyperparathyroidism (sHPT), an increased bone turnover, and a decreased bone mineral density, as well as concomitant skeletal abnormalities consistent with rickets including increased osteoid volume, cortical thinning and growth plate abnormalities during few weeks postnatally when kept on a normal mouse chow [9,10,11]. Here, VDR is linked to secondary hyperparathyroidism.