Several biological and molecular candidates have been tested including EGFR protein expression, truncated receptor variants, such as EGFRvIII, or mutations at the level of EGFR gene or downstream, such as KRAS, but thus far none of them has been proven effective in predicting response (or resistance) to cetuximab in HNSCC (68–71). This evidence concerns the gene EGFR and head and neck squamous cell carcinoma.