CYP27B1 and vitamin deficiency: Its immediate precursor, 25(OH) Vitamin D, is considered to be an adequate marker of vitamin D state [6], but not necessarily of vitamin D physiologic activity because a genetic-induced reduction of 1–25(OH) vitamin D synthesis may result in a functional deficit of vitamin D, as occurs in vitamin D-dependent rickets type I. However, in a recent study, the CYP27B1-1260 promoter polymorphism (rs10877012) also included in our study is not related with vitamin deficiency in children [26].