Recently, cancer immunotherapy using intratumoral injection with the Toll-like receptor 3 (TLR3) agonist, poly I:C double-stranded RNA, was shown to induce an IFNγ-gene expression signature and converted the B16 melanoma immunosuppressive TME to a pro-inflammatory phenotype including greater levels of S100A9 positive TANs [74], indicative of N1 neutrophil infiltration. Here, TLR3 is linked to cancer.