The recent findings that HR-deficient cancer cell are dependent on repair executed by Pol θ suggest that HR and MMEJ can act on similar substrate [44], and there may be a constraint or a complementary relationship between Pol θ and HR pathway, perhaps these studies may explain our findings that co-knockdown of BRCA2 and POLQ can efficiently synergize with cisplatin to inhibit survival of cisplatin-resistant lung cancer cells. The gene discussed is BRCA2; the disease is lung cancer.