Hypoxia, cytokines such as IL-4 and IL-13 (produced by T helper (Th)2 cells) or IL-10 (produced by Treg), metabolic products of tumor cells, and immune complexes may determine the functional phenotype of TAMs: they can be polarized within “classical” or “pro-inflammatory” M1 macrophages, which switch their metabolism towards enhanced anaerobic glycolysis, pentose phosphate pathway activation, and protein and fatty acid synthesis under the influence of interferon (IFN)-γ, NF-κB, STAT-1, and IRF-5. The gene discussed is NFKB1; the disease is neoplasm.