Th17- and Th2-mediated inflammatory pathways are regulated reciprocally during asthma (8), thus, inhibition of type 2 cytokines, such as IL-4 or IL-5, or administration of corticosteroids leads to reorganization of immune response from Th2-mediated eosinophilic to Th17-mediated neutrophilic disease (9, 10). The gene discussed is IL4; the disease is asthma.