Figure 4.
Selective killing of BRCA1/2-deficient cells by different DDR targeted drugs. Both PARPi and REV1i render the ssDNA gaps in BRCA1/2-deficient cells persistent, promoting DSBs or replication catastrophe. POLθi blocks MMEJ and prevents alternative repair of DSBs in HR-defective cells, rendering DSBs persistent in BRCA1/2-deficient cells.
