In this study we show, in both a spontaneous breast cancer model in which the Snail1 gene was genetically deleted in tumor cells and an orthotopic syngeneic transplant model comparing SNAIL1-containing with SNAIL1-depleted tumor cells that the presence of SNAIL1 in breast tumor cells regulates secretion of inflammatory mediators that influence the polarization of the TAMs to a tumor promoting phenotype. The gene discussed is SNAI1; the disease is neoplasm.