Exhausted CD8+ T cells express β1‐AR in response to stress‐associated catecholamines, inhibiting their function and accumulating around sympathetic nerves, but blocking β1‐adrenergic signaling can slow T‐cell exhaustion, enhance anti‐tumor function, and synergistically promote effector T‐cell responses with ICIs therapy.29 Here, ADRB1 is linked to neoplasm.