In most HNSCC, the tumor suppressor p16 is inactivated, resulting in aberrant cell cycle control and cell proliferation, a deficiency in cell senescence, and ultimately dysplasia.165 Similar to HNSCC, OSCC frequently has a low level of p16.166,167 OSCC patients with inactive p16 tend to have a lower survival rate than those with normal or augmented p16 levels.168. Here, CDKN2A is linked to head and neck squamous cell carcinoma.