Beyond promoting GBM cell survival and invasiveness via specific EV proteins (e.g., annexin A1, actin-related protein 3, integrin-β1, insulin-like growth factor 2 receptor, and Alix) [109], GBM-derived EVs play a significant role in creating an immunosuppressive environment that supports tumor growth and resistance to therapy. The gene discussed is ACTR3; the disease is glioblastoma.