Accumulating evidence has shown that ATRis prevent cellular recovery from PARPi toxicity in BRCA1/2-deficient cancer cells by premature mitotic entry with unrepaired DNA damage and by degrading ssDNA gaps [30, 32], indicating that ATRi/PARPi combination exhibited synergistic cytotoxicity in BRCA1/2-deficient background. The gene discussed is BRCA1; the disease is cancer.