Although children with severe asthma have eosinophilic inflammation, high-dose steroids effectively suppress Th2-type cytokines, such as IL-13 and IL-5, but symptoms remain with persistent eosinophilia (Bossley et al., 2012), thus raising the importance of identifying other less steroidsensitive, non-Th2 mediators driving disease. The gene discussed is IL5; the disease is asthma.