Notably, unlike most cancers, where tumorigenesis is generally driven by cancerogenic mutations, the onset of HNSCC tends to be associated with the inactivation of cancer suppressor gene, as in the case of early-stage CDKN2A and TP53 (encoding p16INK4A and p53, respectively) and later-stage PTEN (encoding phosphatase and tensin homologous) (5–7). This evidence concerns the gene CDKN2A and cancer.