Xu et al. [9] detected inflammation and mucin in the airways of mice treated with PM and necroptosis inhibitors and found that necroptosis inhibition could reduce lung inflammation and the excessive secretion of airway mucus in mice—that is, necroptosis contributes to the pathogenesis of PM-induced lung injury, which suggests that necroptosis is closely related to airway inflammation and mucus overproduction in COPD. This evidence concerns the gene MUC5AC and chronic obstructive pulmonary disease.