EGFR and MET are examples of receptor tyrosine kinases (RTK) that can become hyperactive through receptor clustering when overexpressed in HNSCC, but non-RTK oncogenes can also drive HNSCC, including PIK3CA, which is mutated and amplified at a higher prevalence, around 35%, in HNSCC [55], and the oncogenic chloride channel ANO1/TMEM16, a core element of the 11q13 amplicon, is found in a quarter of HNSCCs and more than half of ESCCs [56,57]. This evidence concerns the gene MET and head and neck squamous cell carcinoma.