Tissue levels of 1,25(OH)2D were normal in the DBP KO mice, and markers of vitamin D function such as expression of intestinal TRPV6, calbindin 9k, PMCA1b, and renal TRPV5 were maintained despite having very low levels of serum 25OHD and 1,25(OH)2D and increased loss of these metabolites in the urine.(38) Moreover, injection of 1,25(OH)2D into these DBP KOs showed a more rapid increase in the expression of Cyp24A1, TRPV5, and TRPV6 than in DBP intact controls.(39) However, on a vitamin D‐deficient diet, they quickly developed vitamin D deficiency. The gene discussed is DBP; the disease is vitamin D deficiency.