Preclinical studies have demonstrated that combining ATRi and PARPi enhances cytotoxicity not only in HR‐deficient tumors but also in HR‐proficient cancers with inherent replication stress, such as oncogene‐driven malignancies.[37, 51, 52, 53] This synergy arises from simultaneously disrupting single‐strand break (SSB) repair (via PARP inhibition) and replication stress management (via ATR inhibition), creating a broader therapeutic window. The gene discussed is PARP1; the disease is cancer.