DNA lesions caused by PARP inhibitors lead to increased crossovers. DNA breaks are detected by PARP1 and PARP1 is active in response to DNA breaks. In the cells with intact PARP1 activity, the ssDNA is efficiently repaired (A). However, when the PARP1 activity is inhibited, unrepaired ssDNA breaks can be converted into elongated ssDNA (B) or subsequently into DSBs due to replication collapse (C). Both DNA structures stimulate SCE via HR.