M2‐TAMs facilitate tumor growth by releasing anti‐inflammatory cytokines and angiogenic factors that suppress anti‐tumor immune responses.[65] Hence, we propose that targeting VTN may enhance the efficacy of anti‐PD‐1 therapy by inhibiting TAMs from polarizing toward M2‐type macrophages, thereby alleviating the pro‐cancer effects of the immunosuppressive microenvironment to some extent. The gene discussed is VTN; the disease is neoplasm.