In emphysema animal models, the proliferation, secretion, and adhesion of bone marrow EPCs decreased, with the expression of senescence marker p16 (INK4a) in bone marrow EPCs and lung tissues increasing, while the stem cell antigen 1 (Sca-1) and c-Kit expression decreased [18]; meanwhile, the fact that cigarette smoke extract (CSE) can directly induce the dysfunction of EPCs cultured in vitro and the changes in the expression levels of the above-mentioned gene suggest that EPC senescence and EPC gradual exhaustion exist in smoking-related COPD [18–20]. Here, CDKN2A is linked to chronic obstructive pulmonary disease.