In lung cancer models, the administration of synthetic or bacterial-derived TLR2 ligands induces the differentiation of monocytic myeloid derived suppressor cells (M-MDSC) toward the anti-tumoral M1 phenotype, with the production of IFN-γ, nitric oxide (NO), and pro-inflammatory cytokines such as TNF-α, IL-12p40, and IL-12p70, suggesting a correlation between TLR2 activation and a better anti-tumor response [26,27]. This evidence concerns the gene IFNG and lung carcinoma.