1α, 25-Dihydroxyvitamin D3 [1α, 25 (OH) 2D3] is involved in biological actions such as calcium homeostasis, cell proliferation, and cell differentiation, to many target tissues [1, 2]. In bone formation and metabolism, in particular, 1α, 25 (OH) 2D3 has long been believed to be a prime regulatory factor [3]. That vitamin D deficiency causes rickets, with impaired bone formation and metabolism is well documented. The effects of vitamin D on bone tissues have been intensively studied. For example, by in vitro co-culturing with osteoblasts, cytodifferentiation of osteoclasts from their precursor cells in spleen has been shown to be induced by 1α, 25 (OH) 2D3 [4, 5], indicating a significant role of 1α, 25 (OH) 2D3 in osteoclast differentiation. Thus, despite the accumulating findings of 1α, 25 (OH) 2D3 action on bone, its direct effect on bone tissue in intact animals is still elusive because exogenous 1α, 25 (OH) 2D3 has an indirect influence on bone tissue through fluctuating concentrations of serum calcium. To investigate the action of 1α, 25 (OH) 2D3 on bone tissue of intact animals, we generated mice lacking the vitamm D receptor (VDR) by targeted gene disruption and analyzed the bone phenotype in these mice.