As expected, pathways involved in initiation, progression and maintenance of HNSCC,37,38 such as those associated with AKT, JNK, IL-6/STAT3, ILK, RAS, MAPK/ERK, p38/PAK, TGFβ, PI3K/mTOR and WNT signaling, were among the most significantly upregulated molecular axes in OSCC patients compared to normal controls (Figure 1a). This evidence concerns the gene STAT3 and head and neck squamous cell carcinoma.