Conversely, reduced apoptosis through a lack of pro-apoptotic p53 expression [10] and an increase in anti-apoptotic Bcl-xL and the cytoplasmic form of p21CIP1/WAF1 has been reported in AM from smokers in association with chronicity of inflammation in COPD pathogenesis [11]. Here, BCL2L1 is linked to chronic obstructive pulmonary disease.