It has been demonstrated that the inflammatory response in cigarette smoke-induced pulmonary damage is characterized by an increased number of Th1/Tc1 cells and that IFN-γ is a potent activator of the extrinsic/death receptor and intrinsic/mitochondrial apoptosis pathways and leads to lung inflammation and emphysema associated with induction of matrix metalloproteinase 12 [24]. Here, MMP12 is linked to inflammatory response.