Among the oncogenes of the RAS family, when HRasV12 is overexpressed with activated YAP or with p53 knockdown, both can induce mesenchymal‐like GBM in animal models.[13, 14] Here, to our knowledge, we are the first to report that high expression of TRIM24 combined with the HRasV12 mutation contributes to Ep‐GBM formation, where TRIM24 phosphorylation by activated DNA‐PKcs is the critical link in this process. The gene discussed is PRKDC; the disease is glioblastoma.