However, we did not observe significant augmentation of DNA-damage reagent cytotoxicity during FEN1 inhibition in the RPE1 non-cancer cell lines (Fig. S1f, i and k), suggesting different genetic backgrounds in the cancer and non-cancer cells and lower effects of stress-inducing agents in non-cancer somatic cells, thereby providing a promising approach to glioma clinical treatment. The gene discussed is FEN1; the disease is central nervous system cancer.