Accordingly, NF-κB, in response to activating stimuli such as TLR ligands, IL-1β, and TNF-α, can directly regulate the transition of macrophages toward M1 phenotype, usually exerting a tumor suppressor function, while, in different contexts, NF-κB activation can induce the transcription of many genes responsible for M2 polarization, thus promoting tumor growth (Table 1) [14,51,52,53]. The gene discussed is TNF; the disease is neoplasm.