The conception of the pathogenesis of a disease is probably as important in determining the selection of therapies as is the evidence provided by outcome studies of their efficacy. The recent evolution in our understanding of the pathogenesis of asthma has nicely paralleled advances in clinical research on new forms of treatment. This evolution has occurred so smoothly that we may not be fully aware how far it has taken us. Airflow obstruction is still regarded as the fundamental cause of the characteristic asthmatic symptoms of shortness of breath, chest tightness, and wheezing while the factors leading to airflow obstruction are still assumed to include spasm of airway smooth muscle, thickening of the airway wall, and inspissation of viscid plugs of mucus in the airway lumen. What is new is the recognition of asthma as a chronic disease of the lower airways associated with characteristic inflammatory changes (involving lymphocytes, mast cells, and eosinophils), and possibly irreversible “remodeling” of the airways (by deposition of collagen and proteoglycans, proliferation and transformation of resident cells, and infiltration with inflammatory cells). This modern conception of asthma differs dramatically from the former perception of the disease as an episodic illness characterized by disturbance of the contractile function of airway smooth muscle. The new interpretation has important implications not just for the development of future therapies based on the inflammatory mechanisms involved in the pathogenesis of asthma, but also for the ways in which current therapies should be used.