Given the crosstalk between chemokines and immune cells, we revealed that the secretion of CXCL1/8 and S100A8/A9 by SERPINB3-expressing tumors resulted in increased immunosuppressive myeloid cell infiltration, and these cell populations have been shown to promote tumor progression by disrupting T cell activation signaling (31), facilitating tumor angiogenesis (32), and activating neoplastic cell invasion and formation of a premetastatic niche (33). This evidence concerns the gene CXCL1 and neoplasm.