In summary, we show that MK2 expression in tumour-associated DCs contributes to tumour immune evasion on three levels (Fig. 8): (i) hindering the sustained acquisition of a mature and functional DC phenotype, (ii) dampening an anti-tumour CD8+ T cell response, and (iii) mediating expansion of suppressive myeloid populations at the tumour site. The gene discussed is CD8A; the disease is neoplasm.