However, it remains imperative to acknowledge that merely a minority fraction of cancer patients harbor HR deficiency, thereby constituting the subgroup that stands to gain therapeutic benefits from PARP inhibitor interventions.[13, 14, 15] The therapeutic landscape of other DDR inhibitors has rapidly expanded to target the key sensors of DNA repair and replication, such as ATM, ATR, and WEE1. This evidence concerns the gene PARP1 and cancer.