This is the case (a) in PARPi-resistant BRCA-deficient cancer cells, where ATR inhibition inhibits the restored HR and affects fork protection, thereby resensitizing these cells to PARPi [88], and (b) in cancer preclinical models resistant to PARPi, where CHK1 inhibitor abolishes the resistance by destabilizing replication forks [89]. Here, CHEK1 is linked to cancer.