Similarly, in a mouse model of chronic asthma, the systemic use of Trx1 significantly inhibited airway remodeling, eosinophil infiltration, and AHR while reducing the expressions of eotaxin (an eosinophil chemokine), macrophage inflammatory protein-1 and IL-13 in the lungs; thus, Trx1 improves pathological changes in the airway to prevent remodeling and asthma development (28), in agreement with a recent report which indicated that Trx1 displayed pronounced protective effects on the manifestation of allergic airway inflammation (29). This evidence concerns the gene KMT2A and asthma.