In addition to the interaction between PARP inhibitionand mutations in BRCA1/2, numerous other syntheticlethal interactions have been discovered in cancer.57 In recent years, a number of small molecules targetingDNA damage response have been reported, including inhibitors of DNA-dependentprotein kinase (DNA-PK), ataxia-telangiectasia and Rad3 related (ATR),ataxia-telangiectasia mutated (ATM), CHK1, WEE1, and POLθ, someof which are currently being tested in clinical trials.58−60. The gene discussed is ATM; the disease is cancer.