We favoured to use P465L/wt mutant mice over the more severely compromised PPARγ knock-out mice since it more reliably resembles the situation in chronic inflammatory lung diseases as described, in alveolar macrophages - like in asthma [39], pulmonary sarcoidosis [26,27] and COPD [9] - or in epithelial cells like in cystic fibrosis [40], where PPARγ activation was found to be reduced, but not absent. The gene discussed is PPARG; the disease is asthma.