reduction in exacerbation frequency is not trivial, although it is lower than that anticipated in a population of patients with type 2-high allergic asthma when compared with the effects seen with biologics. In less selected severe asthma populations, such improvements in exacerbation frequency and FEV 1 have formed the basis for the registration of new, long-acting inhaled drugs for asthma. 7,8 Similarly, in chronic obstructive pulmonary disease, such reductions of 15-25% in exacerbation frequency are deemed worthwhile, and led to guideline recommendations for these drugs.Why does the overall effect seem to be as good in noneosinophilic populations as in those with eosinophilia (>250 cells per μL)? Prostaglandin D 2 has broader chemoattractant activity, activating human Th2 cells and macrophages to secrete neutrophil chemokines, and contributes to neutrophilic inflammation in animal models. 9,10 Not all cases of severe asthma or severe exacerbations are eosinophilic, as there are probably multiple pathways towards eosinophilia, and it is conceivable that the activity in the neutrophil pathway at least partially explains the 22% overall exacerbation rate reduction observed in the LUSTER trials. Unfortunately, sputum cell eosinophils and neutrophils were not measured at baseline or during exacerbations in the LUSTER trials. Such information could have proven useful to understanding the results observed.Perhaps, we should not yet close the book on prostaglandin D 2 antagonism, but instead consider adding a new chapter.HAMK reports grants and fees for consultancy or advisory board participation from Novartis, as well as grants and fees for consultancy or advisory board participation from GlaxoSmithKline and Boehringer Ingelheim, and a grant from Chiesi, all outside of the submitted work and all paid to his institution. RG reports grants from Boehringer Ingelheim, Aquilo, Chiesi, and Novartis, outside of the submitted work.