The tumor-derived PMN-MDSCs have been shown to highly produce S100A8/A9, which promotes tumor progression directly by upregulating CXCL1 in tumor cells via the TLR4/p38-MAPK/NFκB pathway, and also indirectly by suppressing glycolysis, proliferation and tumor necrosis factor alpha (TNFα) and interferon gamma (IFNγ) production of CD8+ T cells via the TLR4/AKT/mTOR pathway, leading to anti-PD1 resistance (107). The gene discussed is CXCL1; the disease is neoplasm.