VDR and skin cancer: This raises the question of what function VDR is having on the genome in the absence of 1,25(OH)2D. Moreover, does the much greater percentage of ligand‐independent binding of VDR in the keratinocyte genome relative to the intestinal epithelial cell, osteoblast, or monocyte provide clues to the best characterized ligand‐independent actions of VDR—namely hair follicle cycling and resistance to UVB or chemically induced skin cancer?