Study of an N-nitrosomethylbenzy-lamine-induced ESCC animal model suggested that CCL2-CCR2 signaling activation participates in TAM recruitment into the TME, which can promote immune evasion and tumor progression through the PD-1/PD-L2 pathway, indicating potential intervention and immunotherapy strategies targeting TAMs in patients with ESCC (47). This evidence concerns the gene CCL2 and neoplasm.