Different types of epithelial cells (e.g. human bronchial epithelial cells, mouse lung epithelial cells [MLE]-12, human normal lung epithelial cells) were exposed to CSE or PM to simulate the lung epithelia of patients with COPD who were directly exposed to toxic PM, and treatment with Nec-1 (a RIPK1 inhibitor)/GSK'872 (a RIPK3 inhibitor)/theaflavin-3,3′-digallate (TF-3, which is proven to inhibit necroptosis) remarkably reduced the expression of inflammatory cytokines and mucins that make up the airway mucus. The gene discussed is RIPK3; the disease is chronic obstructive pulmonary disease.