As persistent inflammation and increased TNF-α expression have been contributing to the development of COPD [4;7–11], understanding the molecular mechanisms of TTP downregulation in response to cigarette smoke exposure will definitely benefit the field and could provide new insights regarding therapeutic intervention to reduce inflammation cell recruitment, epithelial cell death, and abnormal enlargement of airspace in COPD patients. Here, TNF is linked to chronic obstructive pulmonary disease.