Neutrophil inflammation stimulated T1 or T17 cell release in T2-low asthma and induced Muc5ac and Muc5b expression in bronchial epithelial cells, which led to goblet cell proliferation, airway remodeling, glucocorticoid resistance, and the occurrence and development of severe or refractory asthma [18]. The gene discussed is MUC5AC; the disease is asthma.