The results showed that several key elements of asthma, including the infiltration of inflammatory cells, especially eosinophils, Th2 cytokines in the BALF, AHR, and specific IgE production were reduced in the CRE-treated miR-33b33, 34, which indicated that the Th2 response plays an important role in the miR-33b-mediated inhibition of asthma development. This evidence concerns the gene AHR and asthma.