LPS-induced TLR4 alone or in combination with IFNγ activates the PI3K-mTOR-AKT (phosphoinositide-3-kinase-mammalian target of rapamycin) pathway, which leads to the polarization of anti-tumor M1 macrophages and the suppression of cancer cell proliferation (79). The gene discussed is IFNG; the disease is neoplasm.