The absence of expression of CD47 on tumor cells increased the expression of tenascin-C in the TME, which in turn triggered TLR4-dependant inflammation in macrophages, characterized by high levels of TNFα secretion and activation of STAT-3 dependent signaling, together with an increased phagocytosis of tumor cells, suggesting an anti-tumor role for this ECM molecule in this model (66). This evidence concerns the gene STAT3 and neoplasm.