The role of adrenergic signaling in tumor immunity remains highly contradictory: activation of β‐AR typically induces the expansion of MDSCs, inhibits the functions of CD8+ T/NK cells, and upregulates PD‐L1 to promote immunosuppression; while agonism of α2‐AR can enhance antigen presentation by macrophages, reduce MDSCs, and activate T‐cell antitumor responses. The gene discussed is ADRB2; the disease is neoplasm.