However, since mutations in both ATM and TP53 is rare in lung cancer cells (Supplementary Fig. 3) and other human tumours (1% of 400 tumours analysed),70 the strategy described here of targeting p53-proficient, ATM-deficient lung cancer cells with the combination of an ATR inhibitor with a PARP inhibitor may have clinical relevance in lung and other cancers. This evidence concerns the gene PARP1 and lung cancer.