Conversely, overexpression of α1-antitrypsin in cigarette smoke-induced and VEGF-inhibition-induced, proteolysis-independent pulmonary emphysema models suggested that α1-antitrypsin serves not only as an inhibitor of elastase but also possesses elastase-independent anti-apoptosis functions in vivo [26], [27]. This evidence concerns the gene VEGFA and pulmonary emphysema.