Studies have shown that downregulation of Sema3E could promote the proliferation and contraction of smooth muscle cells in the airway, increase airway collagen deposition and promote mucus production, which ultimately led to AHR in dust mites sensitized Sema3E-/- asthma model, but after Sema3E treatment, the airway responsiveness was significantly reduced [12]. The gene discussed is SEMA3E; the disease is asthma.