The critical importance of vitamin D in this process is noted in the causal link between vitamin D deficiency and rickets, as well as in studies using genetically modified mice including mice deficient in the vitamin D receptor (Vdr null mice) or in the cytochrome P‐450 enzyme, 25‐hydroxyvitamin D3‐1α‐ hydroxylase (CYP27B1) that converts 25‐hydroxyvitamin D3 to the hormonally active form of vitamin D, 1,25‐dihydroxyvitamin D3 [1,25(OH)2D3] (Cyp27b1 null mice). The gene discussed is VDR; the disease is rickets.