Similarly, the total proteins of RIPK3 and MLKL, downstream of RIPK1, are also increased in the epithelial cells and macrophages of COPD patients, and the knockdown of RIPK1 or MLKL or the use of RIPK1 inhibitors could effectively reduce airway inflammation, remodeling, and emphysema in cigarette smoke extract (CSE)-induced COPD mice [118,119]. The gene discussed is MLKL; the disease is pulmonary emphysema.