It is well established that the development of HNSCC is a multi-step process in which the activation of oncogenes and inactivation of tumor suppressor genes, such as inactivation of tumor suppressor genes p53 and p16 and activation of oncogenes cyclin D1 (CCND1) and epidermal growth factor receptor (EGFR), play critical roles [2], [3], [4], [5]. This evidence concerns the gene TP53 and head and neck squamous cell carcinoma.