To test this hypothesis, we constructed an asthmatic mouse model and an asthma cell model to investigate the interaction among HDAC4, KLF5, Slug and CXCL12 and their effects on airway inflammation and remodeling in vivo and BSMC proliferation and migration in vitro, thereby revealing a pathway does selective vulnerability of asthma. The gene discussed is SNAI2; the disease is asthma.