About the cover: Cover features a diagrammatic representation of a hypothesis of the role of ACE2 (angiotensin-converting enzyme 2) in monocrotaline (MCT)-induced pulmonary hypertension. Normal pulmonary endothelial functions are maintained by a critical balance between angiotensin-converting enzyme (ACE) and ACE2. Monocrotaline treatment impairs this balance by increasing the amount of ACE relative to ACE2, leading to an increase in proinflammatory cytokines and a decrease in antiinflammatory cytokines, resulting in fibrosis and vascular remodeling. This leads to pulmonary hypertension and hypertrophy of the right ventricle. 1-[(2-Dimethylamino) ethylamino]-4-(hydroxymethyl)-7-[(4-methylphenyl)sulfonyl oxy]- 9H-xanthene-9-one (XNT) treatment administered to rats appears to reverse this imbalance by increasing the amount of ACE2 relative to ACE, thus preventing pulmonary hypertension and lung remodeling. For more information, see article by Ferreira and colleagues, beginning on page 1048.