The relevance of these observations is that it enables the simplification of the treatment of asthma for both patients and prescribers, while effectively improving clinically relevant asthma outcomes such as decreasing asthma exacerbations and improving symptoms and airflow obstruction. However, before it becomes widely endorsed as the most effective clinical strategy to prevent and treat asthma exacerbations, there are a number of issues to be considered. First, one needs to recognize the heterogeneity of airway inflammation associated with a loss of asthma control and exacerbations. A patient with an exacerbation associated with eosinophilic bronchitis almost always responds to therapy with an inhaled corticosteroid alone.9A long-acting β2-agonist is not necessary. Despite ex vivo data,10 there is no convincing clinical evidence that a long-acting β2-agonist potentiates the antiinflammatory effect of a steroid.11 A patient with an exacerbation that is associated with neutrophilic bronchitis (usually due to a viral or a bacterial infection) usually does not respond to increased doses of corticosteroids.12There is currently no effective therapy for this phenotype of exacerbation because this has not been investigated. A β2-agonist (rapid or long-acting) may simply provide symptom relief while the exacerbation resolves spontaneously. Since more than half of exacerbations may be noneosinophilic (usually neutrophilic),13 the efficacy may be wrongly attributed to the combination treatment. This can only be resolved if the effect of an antiinflammatory therapy is evaluated using direct measurements of airway inflammation, such as sputum cell counts.14Further, in the same patient, the nature of inflammation may vary with each exacerbation depending on the cause of the exacerbation.15Second, the regular and excessive use of β2-agonists is not without side effects.16 It is, therefore, prudent not to recommend them for all patients with asthma until it is possible to identify the responders and nonresponders, and the patients who are likely to be adversely affected with excessive use of β2-agonists. Also, it is necessary to identify whether it is the corticosteroid or the long-acting β2-agonist in the combination that can be credited with the clinical efficacy.