Here, we document the activation of TINCR expression downstream of P53 activation following UV-induced DNA damage, show increased incidence of SCC in Tincr knockout mice following UV-induced carcinogenesis and describe the presence of loss of function protein-truncating mutations and deletions encompassing the TINCR locus, all in support of a tumor suppressor role in human SCC. The gene discussed is TINCR; the disease is neoplasm.