For example, the prevalence of tumor p16 expression in HPV-positive H&N patients suggests that p16 silencing is not a driver of disease in these patients; in addition, a genome-wide DNA methylation analysis of H&N squamous cell carcinomas found substantial tumor DNA hypomethylation associated with HPV positivity, including hypomethylation of binding sites for the oncogenic transcription factor c-MYC [51]. The gene discussed is CDKN2A; the disease is neoplasm.