Possible mechanistic explanations behind TAM interactions with T cells include the expression of CD39 in TAMs, leading to CD8+ T-cell dysfunction by producing adenosine in cooperation with CD73, as observed in mouse models.68 The secretion of immune-suppressive cytokines such as IL-10 and transforming growth factor-β by microglia can also drive this phenotype in T cells.69 We hypothesize that a highly immune-suppressed TME at the tumour margins is likely to facilitate invasion into the surrounding brain by enabling cancer cells to evade destruction. The gene discussed is IL10; the disease is cancer.