VDR and skin neoplasm: The absolute requirement for VDR for the reduction in DNA damage, together with the apparent ability of these vitamin D–like compounds derived from vitamin D or lumisterol to reduce UV‐induced DNA damage, go some way toward explaining why knockdown of the VDR leads to increased susceptibility to photocarcinogenesis.(50) In contrast, lack of the 1α‐hydroxylase does not apparently increase susceptibility to UV‐induced skin tumors.(52, 85)