The data from both computational and experimental strategies support the hypothesis that the malignant progression of HNSCC is due to, or leads to, multiple genetic and phenotypic defects, such as p53 mutation or underexpression [38,78], and aberrant activation of several major growth factor and cytokine receptor pathways, including the TNF receptor [16], IL1R [9,39], IL6R [31], EGFR [10], hepatocyte growth factor receptor/cMet [41], TGF-β receptor [77], and platelet-derived growth factor receptor [79] pathways. Here, MET is linked to head and neck squamous cell carcinoma.