In the present study we have shown that pharmacological inhibition as well as genetic ablation of AR message significantly (70–90%) inhibited RWE-induced expression of these inflammatory markers in SAEC which suggests that AR is a key mediator in RWE-induced inflammation and inhibition of AR, that we have shown earlier prevents the oxidative stress-induced generation of COX-2 and iNOS, would prevent allergen-induced airway inflammation. The gene discussed is NOS2; the disease is inflammatory response.