In the current study, we found that the overexpression of PRMT6 suppressed TRAF6 transcript levels by facilitating asymmetric dimethylation of histone H3 at arginine 2 (H3R2me2a), which hindered the TRAF6-mediated ubiquitination degradation of EZH2, consequently enhancing the invasion capabilities of glioblastoma cells. The gene discussed is EZH2; the disease is glioblastoma.