This approach creates a pro-inflammatory immune microenvironment in a syngeneic model of GBM by generating obvious increases in CD4+ and CD8+ T cells, while decreasing the number of myeloid-derived suppressor cells and producing cytokines such as interferon (IFN)-γ and tumor necrosis factor-a, thus further enhancing anti-glioma effects (Pituch et al., 2018). The gene discussed is CD8A; the disease is glioma.