Studies have shown that tumor-associated macrophages can induce the expression of pro-inflammatory cytokines and upregulation of PD-L1 in M0 macrophages through IL-6/STAT3 and TLR4 signaling pathways, exerting an immunosuppressive phenotype related to programmed cell death ligand 1 (PD-L1) expression, thereby contributing to the formation of an immunosuppressive microenvironment, which drive ICB resistance [31]. The gene discussed is STAT3; the disease is neoplasm.