First, animals receiving a bolus of exogenous elastase into the lung exhibit lung damage consistent with emphysema, which is progressive [21], and involves many of the main pathophysiologic changes observed in cigarette smoke-induced emphysema in humans and animals, i.e. inflammation, oxidative stress [35], alveolar cell apoptosis [20][21], and MMP-12 induction [21]. This evidence concerns the gene MMP12 and pulmonary emphysema.