Since Th2 cytokines also play vital roles in the pathogenesis of asthma, to exploring how filaggrin expression was regulated in the bronchial epithelial microenvironment by Th2 cytokines and whether the influenced filaggrin level elicited any downstream reaction to maintain the inflammatory response in asthma, we mimicked the Th2 cytokine environment with IL-4 and demonstrated that IL-4 suppressed the expression of filaggrin in bronchial epithelial cell line BEAS-2B cells. This evidence concerns the gene FLG and asthma.