Comparing the airway histology between 21 children with non-eosinophilic asthma to that of 34 children with eosinophilic asthma and 25 non-asthma controls, it was clearly demonstrated that airway remodeling was independent of eosinophilic inflammation, and asthma-relevant mediators such as IL-4, IL-5, and TGF-β [69]. The gene discussed is TGFB1; the disease is asthma.