Moreover, TAMs interact with various tumor cells and trigger multiple signaling pathways via intricate paracrine signals such as IL-6, MFGE8, and CCL5 to boost stem cell self-renewal and resistance to chemotherapy (Gao et al., 2022), with STAT3 serving a dual role as a core molecule that amplifies the immune-suppressive function of TAMs while dampening the anti-tumor immune response (Huang et al., 2020). This evidence concerns the gene CCL5 and neoplasm.