Previous examples of R-loops being involved in the cancer proliferation and progression suggest that targeting transcription-replication conflicts and R-loop formation-associated oncoproteins, such as RNF168, INO80, BRD4, DDX41 and EWS-FLI1, and promoting or inhibiting them may heighten the sensitivity of cancer cells to DNA damage, genomic instability and the immune response, which could ultimately inhibit tumor proliferation to achieve well targeted therapies. Here, RNF168 is linked to cancer.