Due to the fact that activation of toll-like receptors (TLRs) expressed on macrophages results in M1 polarization and robust production of proinflammatory cytokines consisting TNF-α, IFN-γ, and IL-12 through NF-κB pathway, the ability of TLR agonists to reprogram TAM functions in destroying tumor cells have been evaluated in various mouse models. The gene discussed is IFNG; the disease is neoplasm.