Given the limitations of β2-agonist therapy in asthma, including drug tolerance or β2AR tachyphylaxis with repeated use of β2-agonists (25–28), and because EPI can signal through both the β2AR and α1AR (7, 8), here we considered a plausible therapeutic value of α1AR antagonism in preclinical models of β2-agonist insensitivity (29–31). The gene discussed is ADRB2; the disease is asthma.