Thrombospondin-1 can indeed generate enhanced expression of TNFα in bone marrow derived macrophages upon triggering of its receptor CD36, via signaling mediated by TLR4 and NF-κB (63), and the addition of exogenous thrombospondin-1 to a murine macrophage cell line in vitro blocked IL-10 production induced upon ionizing radiations (64), suggesting a tumor-facilitating role. The gene discussed is TLR4; the disease is neoplasm.