Since GBM inhibits the antigen presentation of DCs and the activation of CD8 + T cells through exosomal LGALS9, we propose the hypothesis that when Exos lack LGALS9, immunocompetent mice should be able to not only directly inhibit LGALS9-deficient GL-261 cells but also produce immune memory specific for GL-261 cells. The gene discussed is CD8A; the disease is glioblastoma.