Tumor cells with BRCA1/2 mutations or HR defects are sensitive to PARPis,[35, 36, 37, 38] and recent studies indicated that STAG2 status correlates with treatment response to PARP inhibitors.[39, 40] Since knockout of STAG2 impairs HR activity, we determined whether STAG2 knockout enhances the sensitivity to PARPi. This evidence concerns the gene STAG2 and neoplasm.