For instance, when VEGF, which is abundant in the lungs, is neutralized in animal models, the result is an apoptosis-dependent enlargement of airspaces and structural changes similar to emphysema [25-27], not only by induction of apoptosis of type II pneumocytes but also by impaired production of surfactant [13,28]. The gene discussed is VEGFA; the disease is pulmonary emphysema.