Also, tumor-derived sEVs could polarize macrophages into an immunosuppressive phenotype within the PMN through TLR2-NF-kB-dependent, glycolytic dominant metabolic rewriting by increasing the expression of PD-L1 in TAMs and lactate produced via glycolysis could act on NF-κB, further driving PD-L1 expression [67]. This evidence concerns the gene NFKB1 and neoplasm.