On the other hand, our finding that JAK-STAT6 inhibitors block Th2 cytokine-induced eotaxin-3 expression in esophageal fibroblasts as well as in esophageal epithelial cells suggests a potential therapeutic role for these agents in treating both the epithelial inflammation and subepithelial fibrosis in eosinophilic esophagitis. The gene discussed is STAT6; the disease is eosinophilic esophagitis.