ATM and neoplasm: Studies showing that loss of ataxia-telangiectasia mutated (ATM) kinase, a cardinal kinase in DDR, or deficiency in MutS homologue 3 (MSH3) increases cellular sensitivity to DNA-PK inhibitor (KU-0060648) treatment25–27 suggest that there may be opportunities for combination with other inhibitors of DDR, particularly if those effects are significantly enhanced by tumour-specific DDR deficiencies such as in ATM signalling.