Mechanistically, our results suggest that the selective cytotoxicity of PARPi in HRR-deficient cells is achieved thanks to an optimal combination of (i) higher levels of endogenous DNA damage present in HRR-deficient cancer cells during S-phase, (ii) the PARP1 trapping potency of the PARPi, and (iii) the insufficient DNA repair capability of HRR-deficient cells (Fig. 8K). This evidence concerns the gene PARP1 and cancer.