Studies have indicated that TAMs produce pro-inflammatory cytokine IL-6 to activate the JAK/STAT3 signaling in CRC cells and lead to epithelial–mesenchymal transition (EMT) involved in tumor progression (81), which in turn leads to the CCL2 secreted by CRC cells, to promote macrophage recruitment, while, inhibition of CCL2 or IL6 can break this crosstalk (82). This evidence concerns the gene CCL2 and neoplasm.