In contrast, HNSCC with a much lower EGFR/KRAS mutation burden (2%) (Stransky et al., 2011; McBride et al., 2014; Cancer Genome Atlas Netwrork, 2015) relies more on an overstimulated wild type EGFR/JAK2 pathway for oncogenic signaling (Concha-Benavente et al., 2016). This evidence concerns the gene JAK2 and head and neck squamous cell carcinoma.