Acute symptoms of asthma are largely a consequence of contraction of airway smooth muscle, yet emphasis in asthma pharmacology has shifted away from smooth muscle dysfunction and refocussed upon inflammatory events in the airway mucosa and submucosa. Thus, as described by John Morley, existing anti-asthma drugs are used either to suppress inflammatory events (as preventive therapy), or to relieve obstruction to airflow (as symptomatic therapy). There is now a prospect of novel drugs that, by inhibiting phosphodiesterase isoenzymes selectively, will combine preventive and symptomatic therapies within a single molecule. Since atopy is associated with aberrant expression of phosphodiesterase isoenzymes in mononuclear cells, such therapies may belie their pragmatic origins and be envisaged as targeting a specific molecular defect.