SummaryA substantial proportion of asthma has its origins in childhood but attempts to identify modifiable exposures that trigger asthma inception have yielded disappointing results. It is increasingly recognised that asthma may not be a single disease entity but instead consists of a number of phenotypes that share common features perhaps with different aetiologies and pathophysiological pathways leading to disease.The aim of this review is to describe approaches to defining asthma phenotypes on the basis of clinical and epidemiological data and to consider the clinical implications of the phenotypes described. Differences in clinical features (atopy, lung function, prognosis) have been associated with phenotypes derived from unsupervised statistical approaches to phenotype definitions. Greater understanding of the genetic pathways underpinning asthma has also led to some insights into asthma endotypes that manifest as different clinical phenotypes. However, the challenge to translate these findings into interventions to change the natural history of asthma has yet to be overcome. Technological advances are driving the creation of massive data resources that can be brought to bear on this problem. Whether they will finally solve the problem of phenotypic complexity in asthma remains to be discovered. If they do, the possibility of personalised interventions for asthma may eventually be realised.