In HPV+ HNSCC cases, the expression of viral oncoproteins E6 and E7 leads to binding and targeted destruction of E6 to p53 and E7 to Rb.6,23 Overall, these findings suggest that in at least 80% of HNSCC cancers, the p53 pathway is downregulated or inactivated.22 Furthermore, inactivation of the TP53 gene in HNSCC also accounts for the clinical behavior of tumors in response to therapy, as functional mutations in TP53 have been reported to have a significant impact on survival rate.21 The gene discussed is TP53; the disease is cancer.