STAT3 and neoplasm: CCL2 facilitated the accumulation of polymorphonuclear myeloid-derived suppressor cells (PMN-MDSCs) into the tumor microenvironment and increased MDSC-mediated inhibition of T cells in a STAT3-dependent manner, and blocking CCL2 using antibodies reduced tumor growth and MDSC infiltration in a murine model of colitis-associated CRC [109].