Mucosal inflammation and more recently airway remodeling continue to be a focus of interest when considering both the pathophysiology and treatment of asthma. Although a number of candidate genes relevant to inflammatory cell action have been identified and linked to atopy and airway hyperresponsiveness, it is important to understand genetic factors that might determine the extent of tissue remodeling. The mechanisms regulating the allergic responses in the airways are complex, involving antigen presenting cells and T lymphocytes, which process antigens and orchestrate the response, and mast cells and eosinophils as effector cells. Abundant evidence also points to a proinflammatory role for structural cells, including epithelial and endothelial cells, and smooth muscle. Because of the complex nature of the inflammatory changes in asthma, the exact relation between individual inflammatory cells and their mediators on the one hand and hyperresponsiveness of the airways and clinical manifestations on the other remains unclear. The same applies to the phenomenon of airway remodeling because it is uncertain exactly how the different components of restructuring affect the airway physiology. If progress is to be made in the treatment of asthma, further efforts will be needed to understand the regulation and link between the mechanisms causing inflammation and those leading to fibrotic changes.