CD4 and neoplasm: Therefore, tumor-derived EVs use the above strategies to potentiate the immunosuppressive microenvironment and favor tumor growth by: (1) reprograming macrophages toward a M2 tumor-supportive phenotype [64,65]; (2) inducing cytotoxic CD8+ T cell apoptosis [64], thus lowering NK proliferation; and (3) shifting CD4+ cells to T regulatory lymphocytes [66].