Interfering with molecular partners of MYC to prevent its ability to regulate transcriptional programs is an attractive therapeutic strategy.[69] Current inhibitory strategies targeting M2‐like macrophages mainly including reducing or eliminating tumor‐associated macrophages (TAMs), re‐inducing them into M1‐like macrophages, and promoting the phagocytosis and antigen presentation of TAMs by blocking “don't eat me” signals.[70] In our study, we found that Bindarit, a pharmacological inhibitor of CCL7/CCL8, could effectively inhibit tumor cell recruitment of M2‐like macrophages in vitro. This evidence concerns the gene CCL8 and neoplasm.