Aiming to comprehend if the activated DNA-PKcs arose from DSBs, we selected 155 patients with primary glioma occurrence and null chemo- or radiotherapy before surgery from our glioma cohort, then surveyed the expression of γH2AX. On the contrary to that p-DNA-PKcs levels were positively associated with glioma grades, γH2AX did not appear to be discriminatingly expressed among different grades of glioma tissues (Supplementary Figure S2A). Further analysis certified that there was not correlation between expression of γH2AX and p-DNA-PKcs, suggesting that activation of DNA-PKcs in glioma was not exclusively in response to DSBs (Supplementary Figure S2B). Taken together, these results indicated that p-DNA-PKcs expression was abnormally overexpressed in gliomas and dysregulated expression of p-DNA-PKcs correlated with malignant development and poor prognosis in clinical glioma patients.