The hypothesis that IL-6 might be the primary trigger of the EMT program in HNSCCs is supported by the finding that a main target of the classical IL-6/IL-6R pathway, p-ERK, was upregulated following FbCM treatment and the IL-6 receptor inhibitor, tocilizumab, completely blocked the effects of FbCM on HNSCC cells (Figure 1A and Figure 4C–E). This evidence concerns the gene IL6R and head and neck squamous cell carcinoma.