Recurrent mutation and amplification of PIK3CA (35%) and to a lesser extent HRAS (4%) mutations have emerged as the most frequent oncogenic drivers in both HPV- and HPV + HNSCC, with other potential oncogenic events including EGFR, CCND1 overexpression, or PTEN inactivation27,28. This evidence concerns the gene PTEN and head and neck squamous cell carcinoma.