First, NF-κB is often constitutively activated in cancer through genetic mutations in NF-κB subunits, activation of upstream oncogenic pathways such as epidermal growth factor receptor–RAS or the presence of inflammatory cytokines including TNF-α, interleukin-6, and interleukin-1β in the tumor microenvironment that drive receptor-mediated pathways (44, 45, 46). This evidence concerns the gene TNF and neoplasm.