Treatment of tumor-bearing mice with Sema4D mAb reduced PMN-MDSCs suppressive capacity through inhibition of Sema4D-driven ERK- and STAT3-dependent arginase expression and abrogated PMN-MDSCs recruitment through reducing MAPK-dependent chemokine production by tumor cells in murine oral cancer-1 (MOC1) tumors, which led to enhanced tumor infiltration by CD8+ TIL and activation of tumor-draining lymph node T lymphocytes in response to tumor antigen. The gene discussed is STAT3; the disease is neoplasm.