In conclusion, we demonstrated that blockade of the α1AR abrogated EPI-induced calcium flux, pMLC, and HASM shortening, under experimental conditions that induce β2AR desensitization, providing a basis for reexamining α1AR inhibition for the management of stress/exercise-induced asthma and/or β2-agonist insensitivity in patients with difficult-to-control, disease subtypes. The gene discussed is ADRB2; the disease is asthma.