Exposure to CS can exacerbate airway inflammation in pre-existing asthma, and can also contribute to increased neutrophils and macrophages in lung tissues and decreased histone deacelytase2 (HDAC2) in the airways [28], which leads to airway inflammation in the direction of a non-Th2 phenotype and ultimately ICS resistance [25, 50]. The gene discussed is HDAC2; the disease is asthma.