In HNSCC, NFκB is often aberrantly activated and is a common mediator of the effects of numerous pro-inflammatory cytokines (TNFα and IL-1), as well as other signalling pathways targeted by oncogenic mutations, genetic copy number alterations (CNA), or viral oncogenes [14,19,20]. This evidence concerns the gene NFKB1 and head and neck squamous cell carcinoma.