Building upon this hypothesis, Li and Graeber proposed that, whereas glioma-derived TGF-β exerts immunosuppression by driving alternative polarization in TAMs, TGF-β produced by the glioma TAMs may promote tumor growth and invasion by stimulating the upregulation of its own cognate receptors TBRI and TBRII on glioma cells [29] enabling a more potent trophic response to the high concentration of TGF-β proposed to exist in the glioma microenvironment. The gene discussed is TGFB1; the disease is neoplasm.