Since TLR3 agonists, such as dsRNA fragments, may be consistently present in the HNSCC tumor microenvironment and necrotic fluids, these endogenous DAMPs may create a positive feedback loop by further activating TLR3, potentially driving a pro-tumorigenic effect, as we have previously reported [10]. This evidence concerns the gene TLR3 and head and neck squamous cell carcinoma.