Since PARP1/2 are enzymes that facilitate SSB repair, excisional base repair, and homologous recombination, their additional inactivation in tumor cells allows, effectively, the blocking of repair mechanisms in addition to the repairing of defects, resulting from mutations in the subunits of chromatin remodeling complexes, and contributes to the development of a synthetic lethality of tumor cells [233]. This evidence concerns the gene PARP1 and neoplasm.