Therapeutic agents designed to deplete the MDSC population (i.e., gemcitabine and peptibodies), block their recruitment to the tumor site (i.e., anti-CCL2 and anti-CCR5), promote their differentiation (i.e., ATRA and vitamin D3) or inhibit MDSC-mediated immunosuppression (i.e., anti-CCL2 and anti-CCR5) have been extensively reviewed in the literature (88, 89, 93). Here, CCL2 is linked to neoplasm.