Vitamin D functions by stimulating intestinal calcium and phosphorus absorption, by stimulating bone calcium mobilization, and by increasing renal reabsorption of calcium in the distal tubule. These functions on bone and possibly kidney, but not intestine, require the parathyroid hormone. As a result of these functions, serum calcium and phosphorus concentrations are elevated to supersaturating levels required for the mineralization of bone to prevent rickets, osteomalacia, and hypocalcemic tetany. Recent experiments demonstrate that maintaining serum calcium and phosphorus levels in vitamin D-deficient rats in the normal range results in normal bone growth and mineralization. However, increased calcification results because bone resorption by osteoclasts is a vitamin D-dependent process. Thus, bone resorption, modeling and remodeling must be considered vitamin D-dependent processes. Vitamin D must be metabolized to 25-hydroxyvitamin D3 by the liver and subsequently by the kidney to 1,25-dihydroxyvitamin D3 before function. 1,25-Dihydroxyvitamin D3 is metabolized to a C-23 carboxylic acid (calcitroic acid) but the pathway is unknown. Although 25-hydroxyvitamin D3 is metabolized to 24R,25-dihydroxyvitamin D3, 25,26-dihydroxyvitamin D3 and 25-hydroxyvitamin D3-26,23-lactone, these pathways play no role in the function of vitamin D as shown by appropriate fluoro analogs of 25-hydroxyvitamin D3. 1,25-Dihydroxyvitamin D3 binds to a specific receptor in the intestinal nuclei to elicit a stimulation of calcium transport. 1,25-Dihydroxyvitamin D3 plus the receptor causes transcription of specific genes that code for calcium and phosphorus transport proteins. Only one protein, the calcium binding protein, has been identified as being vitamin D dependent. Two others have been described, but no clear description of the molecular mechanism of action of 1,25-dihydroxyvitamin D3 is yet available.