We also discovered that VDR regulated the expression of long non‐coding RNAs (lncRNAs) such that in the Vdr null mouse epidermis the balance between oncogenic and tumor suppressor lncRNAs was shifted to oncogenic species.(67) Additionally, we(63) noted a reduction in clearance in cyclobutane pyrimidine dimers (CPD) after UVB exposure of the skin of Vdr null mice, suggesting that disruption of DNA damage repair was playing a role in tumor susceptibility in these mice. The gene discussed is VDR; the disease is neoplasm.