Although the precise mechanisms in DMGs remain to be fully elucidated, it has been shown that GBM tumour cells recruit and polarise both macrophages and microglia to an M2 phenotype, resulting in the inhibition of T cell proliferation through the production of the immunosuppressive cytokines TGFβ and IL-10 [274], whilst also preventing the production of cytokines required to support activated tumour-specific CD8+ T, CD4+ Th1 and Th17 cells [247]. The gene discussed is CD8A; the disease is glioblastoma.