β2‐AR,[38] while another report has shown that β1‐AR blockade suppresses neutrophil activation thus reduces the brain‐damaging effects.[39] In acute phase of inflammation, β2‐AR acts as co‐activator to enhance TLR pathway's response to LPS in innate immune cells and promote IL‐10 autosecretion to further modulate the inflammatory response,[40] while during the long‐term reparative phase, chronic activation of β2‐AR on myeloid cells is implicated to fibrotic process following myocardial infarction (MI) with up‐regulation of Anax1. Here, ADRB2 is linked to myocardial infarction.