It is generally accepted that tumour-cell-derived EVs can participate in immune evasion strategies, by reducing the antigen presentation capacity of DCs [60], inhibiting T-cell activation by releasing PD-L1 containing EVs [61,62], or steering the differentiation of macrophages towards a tumour-promoting (M2) phenotype [63]; functional studies have shown that tumour-cell-derived EVs can also contain immunogenic molecules, and facilitate the transfer of tumour-associated antigens and DAMPs to DCs, increasing the cytotoxicity of T cells and NK cells [64,65,66]. The gene discussed is CD274; the disease is neoplasm.