Several studies have previously documented the prevalence of constitutive activated NF-κB in diverse HNSCC cell lines and tumor tissues specimens [9–12], and this dysregulated NF-κB signaling contributes to the cell survival, angiogenesis, migration, tumorigenesis, and therapeutic resistance of HNSCC [13–15]. This evidence concerns the gene NFKB1 and head and neck squamous cell carcinoma.