A study discovered that CD300ld was specifically expressed and upregulated on PMN-MDSCs after tumor occurrence; these cells recruited PMN-MDSCs into tumors through the STAT3-S100A8/A9 axis and inhibited T-cell activation.221 Interestingly, the deletion of CD300ld did not affect the development of mice and could synergistically inhibit tumor growth in conjunction with anti-programmed cell death-1 (PD-1) treatment.221 Therefore, combining drugs targeting key components of the S100A8/A9 signaling pathway with various antitumor therapies may represent a promising treatment strategy in the future. The gene discussed is PDCD1; the disease is neoplasm.