We then transiently transfected RNF168 into U87/G0S2 and LN229/G0S2 cells, and found that ectopic expression of RNF168 inhibited 53BP1 expression (Fig. 6b) and 53BP foci cell formation (Fig. 6c and d) upregulated by G0S2 overexpression in indicated glioma cells compared to the controls at 8 h post IR, whereas it increased γ-H2AX expression (Fig. 6b) and γ-H2AX foci cell formation inhibited by G0S2 overexpression (Fig. 6c and e). Here, H2AX is linked to glioma.