On the basis of our findings, we speculate that DTX3L and XPO1 facilitate TIRR nuclear export and degradation upon DNA damage (Fig. 8a) and that elevated DTX3L expression induces HR deficiency by promoting TIRR degradation and subsequently sensitizes cancer cells such as prostate cancer cells to synthetic lethality by PARP inhibitors (Fig. 8b). This evidence concerns the gene DTX3L and prostate cancer.