In preclinical studies, loss of ATM signalling (e.g., through ATM or p53 deficiency, or tumour protein [TP53] mutation) has been reported to drive reliance on ATR in response to DNA damage;7,10–12 subsequent loss of ATR signalling has been shown to result in synthetic lethality.7 ATR inhibition is an attractive therapeutic target for cancers in which DNA-damaging chemotherapy is utilised as standard therapy, but which retains a substantial unmet need.13 Here, ATM is linked to cancer.