Secondly, DDR inhibition can result in sensitization by exploiting synthetic lethality, as shown in the context of poly(ADP-ribose)-polymerase (PARP) inhibition in tumors deficient in HRR as well as by ATR blockade in replication-stress-adapted tumors, and, thirdly, by causing a higher tumor mutation rate as a failure of DNA damage repair results in elevated neoantigen expression in line with increased cytotoxic T lymphocyte activity [18, 21]. The gene discussed is ATR; the disease is neoplasm.