Due to its overexpression or upregulated activity in HNSCC, the EGFR is the most investigated molecular target, and some strategies to decrease its overexpression have demonstrated reliability in vitro, such as nuclear Ca2+ depletion [5] or the blockage of the EGFR downstream proliferation axis by using the monoclonal antibody Cetuximab, one of the immunotherapies approved for the treatment of recurrent/metastatic HNSCC. This evidence concerns the gene EGFR and head and neck squamous cell carcinoma.