Increasing the DNA DSB burden in cancer cells via PARP1 inhibition is crucial in the treatment of tumors harboring mutant breast cancer susceptibility genes 1 and 2 (BRCA1 and BRCA2).10 They are tumor suppressors with involvement in multiple intracellular pathways, most important of which is the role of regulating the DNA damage repair defect (DDR).11 This evidence concerns the gene PARP1 and breast cancer.