Genotypic and phenotypic factors can influence the response to drug treatment for asthma [
23,
26,
27,
83]. For example, adrenergic β
2-receptor polymorphisms, particularly variants at position 16 (Gly16Arg) and 27 (Gln27Glu), have been associated with impaired bronchodilator response to short and long-acting β
2-receptor agonists and naturally occurring mutations in the promoter of 5-lipoxygenase gene (ALOX5) may influence the clinical response to drugs modifying the 5-lipoxygenase pathway [
84‐
86]. Several inflammatory phenotypes, which have been identified mainly on the basis of induced sputum cell profiles, influence the response to drug treatment [
87,
88]. For example, sputum eosinophilia predicts corticosteroid responsiveness [
89‐
93] and the response to the anti-IL-5 blocker mepolizumab in severe asthma [
26,
27]. Non-eosinophilic asthma, a term used to describe an absence of raised numbers of inflammatory cells (also known as paucigranulocytic inflammation) or neutrophilic inflammation, responds less well to inhaled corticosteroids [
91‐
93]. Macrolides may be effective in neutrophilic asthma [
94]. Th
2-high asthma, as defined by gene expression analyses of airway cells, predicts an improvement in lung function with inhaled corticosteroids in patients with mild to moderate disease, whereas patients with Th
2-low asthma respond poorly to inhaled corticosteroids [
95]. The development of novel therapies for severe asthma in the future is likely to involve genotypic and/or phenotypic assessment to identify patients who will gain the most from a specific intervention.