CD86 and neoplasm: Although the function and phenotype of activated DCs is generally determined by co-stimulatory molecules (CD80, CD86) and chemokine receptors such as CCR7 [194, 195], the immunological function of DCs could be influenced by multiple factors within TME, which is partly modulated by epigenetic regulations and being considered as the potential targets to elevate immune surveillance and enhance anti-tumor immunity [196].