Despite these positive changes in the TME after TLR agonist administration, there are some tumor cells that express—and are activated—by TLR ligation (127, 131), which promotes tumor growth and chemoresistance in TLR7/TLR8 overexpressing human pancreatic cancer cells (132) and production of immunosuppressive cytokines (TGF-β, vascular endothelial growth factor (VEGF), IL-8) and resistance to apoptosis in human lung cancer cells (133). Here, VEGFA is linked to lung carcinoma.