The restoration of HR competency and replication fork stabilisation (fork protection) has been described as two critical compensatory PARPi- resistance mechanisms.9,10 As the damage induced by PARP inhibition is generated during the S phase, PARPi-treated cells rely heavily on the DDR protein ATR (ataxia telangiectasia and Rad3-related), which plays a major role in survival during DNA replication stress.9,10 ATR inhibition significantly enhanced the cytotoxicity of PARPi, not only in BRCA-mutated but also in BRCA-proficient and PARPi-resistant human cancer cells.10–13. This evidence concerns the gene ATR and cancer.