PARP1 and cancer: Beyond classic DDR targets, modality-expanding approaches are emerging: 2-chloro-N,N-diethylethanamine hydrochloride (CDEAH), a guanine-alkylating agent, preferentially kills PARP1-deficient cells by forcing dependence on BER and NER and shows combination potential with PARP inhibition [209]; and cancer-specific INDEL attacker (CINDELA) leverages CRISPR–Cas9 to inflict multi-site DSBs specifically at mutated sequences, offering a blueprint for truly personalized, genotype-directed cytotoxicity [210].