Contrary to previous reports that mice treated with a small-molecule MAP3K19 inhibitor demonstrated significantly suppressed bleomycin-induced pulmonary fibrosis and cigarette smoke-induced inflammation and emphysema [3,4,5], our findings suggest that MAP3K19 knockout resulted in progressive OVA-induced allergic airway inflammation, without increased AHR, in the murine model. Here, AHR is linked to pulmonary emphysema.