While analyses of EGFR gene copy number and protein expression in patient tumors have not been found to be predictive of cetuximab response [92,93], a well-established intrinsic or acquired resistance mechanism to anti-EGFR therapy in HNSCC is the compensatory activation of alternate receptor tyrosine kinases (RTKs) including c-Met. This evidence concerns the gene MET and head and neck squamous cell carcinoma.