In 2009 we created novel transgenic mice that allowed us to show that the single most important role for vitamin D during growth is to support intestinal calcium absorption; all other phenotypes of vitamin D deficiency are secondary to the loss of efficient calcium absorption.  In addition, we also showed that the calcium apical membrane calcium channel TRPV6 is a critical part of the intestinal calcium absorption mechanism and we have shown that vitamin D regulates calcium in the lower bowel and this contributes to the acquisition of peak bone mass.  More recently we used genomic approaches to explain why the intestinal vitamin D receptor gene expression is higher than other tissues.  We also demonstrated that there are intestine segment and compartment-specific patterns of vitamin D induced gene expression and that the breadth of vitamin D action indicates roles beyond the control of calcium metabolism.