ATR and neoplasm: Although ATR is crucial for repairing DNA damage caused by olaparib, we now propose that HG-SOC cells, expressing endogenous ETAR, are particularly sensitive to ATR inhibitor treatments because ATR inhibition counteracts the olaparib-induced transcription of ETAR. HG-SOC cells overexpressing ETAR are less prone to olaparib, suggesting that the ETAR expression level might predict patients’ tumour sensitivity to the combination of ATRi and PARPi treatment.