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. Here, EDNRA is linked to neoplasm.