Recruitment of ARID1A to double strand DNA breaks facilitates efficient processing of DNA ends, producing single stranded DNA which becomes coated in replication protein A, thereby sustaining the DNA damage signal and promoting cycle arrest.8 A number of novel therapeutic strategies are currently being trialed for ARID1A defective cancers, including poly-ADP ribose polymerase (PARP) inhibitors (NCT03682289), phosphatidylinositol-3-kinase inhibitors (NCT03842228), and bromodomain containing protein 4 (NCT03297424) inhibitors, alongside ATR inhibitors (NCT03682289). The gene discussed is ATR; the disease is cancer.