M2-like TAMs induce resistance to ICB therapy in solid tumors, the underlying mechanisms include, but are not limited to, recruitment to the TME via tumor-derived chemokines, such as CXCL8 and CCL2, to mediate local immunosuppression, as well as the direct expression of high levels of PD-L2 but not PD-L1 to escape anti-PD-1 targeted therapies (30, 31). The gene discussed is CXCL8; the disease is neoplasm.