These observations could be an instrumental step to improve the efficacy of PARP inhibition in ovarian cancer [42–45] showing that, beyond modulating ATR/CHK1 or ATM/CHK2 [46–48], STAT3 exerts a role downstream of the olaparib-induced DDR pathway, regulating the transcription of ETAR, identified as key vulnerability in response to DNA damage. The gene discussed is CHEK2; the disease is ovarian carcinoma.