Because our data indicate that HDM activates the NLRP3 inflammasome in macrophages and induces IL-1β secretion in the lungs, we hypothesized that the NLRP3/IL-1β signaling pathway is the main driver of LC progression in response to chronic HDM exposure in our mouse models. The gene discussed is NLRP3; the disease is laryngotracheoesophageal cleft.