Because CtIP (CtBP-interacting protein), which functions in the initial step of HRR with NBS1 and BRCA1 by acting as an end-resection enzyme to produce 3′-single stranded DNA, is known to be frequently downregulated in breast cancers as well as in other types of cancers, we focused on CtIP in this study and showed that breast cancer cells with defects in CtIP function are hypersensitive to the PARP inhibitors olaparib and veliparib. Here, PARP1 is linked to cancer.