As an example of how this may be effective, it has been demonstrated that TLR-4 activation, using the chemotherapeutic agent paclitaxel, was able to polarise immunosuppressed M2 macrophages towards an M1 state, with their inflammatory activation able to inhibit tumour progression in both breast cancer and melanoma models, with TAMs isolated from tumour-bearing mice treated with paclitaxel exhibiting an increase in M1 phenotype iNOS, IL-6 and IL-12 expression concurrent with decreased M2 phenotype expression of CD206 and Arg-1 [259]. This evidence concerns the gene TLR4 and neoplasm.