In PARP inhibitors-resistant but BRCA-mutant ovarian cancer cells, both fork protection functions of BRCA1/2 and HR are sequentially bypassed, and cells become increasingly dependent on ataxia telangiectasia and Rad3-related kinase (ATR) for recruitment of RAD51 onto DSB and stalled forks. This evidence concerns the gene PARP1 and ovarian carcinoma.