We demonstrated that ID8 cells produce MCP1 and that conditioned media from such cells promotes the conversion of RAW 264.7 cells to an arginase expressing M2 phenotype, while in vivo inhibition of thrombin with dabigatran etexilate significantly reduced levels of MCP-1 in the ascites of ID8-tumor bearing mice as well as populations of Gr-1+CD11b+ and CD11c+CD11b+ myeloid cells. This evidence concerns the gene CCL2 and neoplasm.