Tumor-derived sEVs increase macrophage glycolysis through TLR2-NF-kB signaling to make them obtain immunosuppressive phenotype, which was distinguished by abundant (programmed cell death ligand-1) PD-L1 expression and PD-L1 was positively relevant with levels of GLUT-1 from primary tumors [67]. Here, NFKB1 is linked to neoplasm.