The airways of chronic smokers and COPD patients are characterized by structural changes to the airway epithelial cells that contribute to airflow obstruction, such as: increased mucus production and secretion, particularly MUC5AC which is increased in COPD airways, decreased mucus clearance through ciliated cell dysfunction, and decreased ion channel activity, partly due to decreased expression of channels such as CFTR, leading to decreased airway hydration which normally thins mucus and makes it easier to clear [3,6,7]. The gene discussed is CFTR; the disease is chronic obstructive pulmonary disease.