Subsequently, platelet–neutrophil interaction fostered mutual activation and neutrophil extracellular traps and triggered the release of platelet granule contents and the generation of lipid mediators, which affected the functions of various effector immune cells including T-helper, CD8+ T and natural killer cells in the tumor environment via various cytokines, chemokines and prostaglandins signaling such as Toll-like receptors, interleukin-1 (IL-1), IL-17, CCL2, IL-8, PD-L1, IFN-γ, and TNF-α, etc., facilitating immune evasion of cancer cells and tumor development and dissemination [33]. This evidence concerns the gene CCL2 and neoplasm.