CD226 and neoplasm: Moreover, many evidences support the idea that DDR can be frequently activated in early neoplastic lesions, and probably NKG2D and DNAM-1 ligand induction by DNA damage represents a tumor surveillance mechanism operating at the very early stages of tumorigenesis, possibly increasing the sensitivity of damaged cells to NK- and/or T cell-mediated lysis (11, 63–66) (Figure 1).