These findings are consistent with previous studies that have highlighted the central role of Th2 cytokines (e.g., IL-5, IL-13) and Th17-related cytokines (e.g., IL-17A, IL-22) in the pathogenesis of asthma, leading to eosinophilic and neutrophilic inflammation in the airway, and consequently promoting airway hyperresponsiveness and remodeling (22–28). The gene discussed is IL13; the disease is asthma.