Because inhibition of DNMT activity using 5-aza before sensitization in a mouse model of experimental asthma alleviated allergic asthmatic features including lung inflammation, mucus production and AHR77, the exacerbated asthma features we observed in HDM-challenged Tet1−/− mice compared to the HDM-challenged Tet1+/+ mice are unlikely due to the downregulation of Dnmt1, Dnmt3a, and Dnmt3b. The gene discussed is DNMT3A; the disease is asthma.