In fact, EMT and TAMs provide invasive and metastatic capabilities to tumor cells and modulate the tumor microenvironment, leading to the suppression of anti-cancer immune response, and limiting the effects of cytotoxic chemotherapy.6–11 TNBC, which is often characterized by the presence of both EMT and TAMs, is a good model to explore potential molecular markers maintaining the biological intersections between these two signalings.9–12 In this study, we demonstrated that the receptor AXL was the most significant EMT-related kinase associated with macrophage cells in the tumor stroma of TNBC. The gene discussed is AXL; the disease is cancer.