Conversely, 53BP1 pathway-associated DSB repair activities underlie the synthetic lethal effect of poly-ADP ribose polymerase (PARP) inhibitor (PARPi) treatments in BRCA1 mutation-associated cancers: genetic ablation of 53BP1 pathway components results in PARPi resistance in cellular and tumour models of BRCA1-deficiency9,20,21. This evidence concerns the gene BRCA1 and neoplasm.