In our previous studies, we found that in mutant mouse models with genetically deleted 1α(OH)ase (1α(OH)ase−/−) or VDR (VDR−/−), osteoblast numbers, mineral apposition rate, and bone volume were suppressed below levels seen in wild‐type mice (Panda et al., 2004), even when hypocalcemia and secondary hyperparathyroidism were prevented by feeding the animals a high calcium, high phosphorus, lactose‐containing “rescue” diet. This evidence concerns the gene VDR and secondary hyperparathyroidism.