Of the genetic or epigenetic alterations known in HNSCC, one of the most frequently altered pathways is EGFR/Ras/PI3K, which, along with other pathways (p53/DNp63, pRb/CycD1, TGF-β/Smad and NF-κB), can lead to Akt dysregulation which has indeed been found in 20~60% of tumor samples and in the majority of HNSCC-derived cell lines25, 27, 28, 29. Here, TGFB1 is linked to neoplasm.