Remodeling of the arterial wall occurs mainly as a consequence of increased wall stress caused by hypertension. In this issue of the JCI, Azizi et al. report that in humans with a kallikrein gene polymorphism that lowers kallikrein activity, the brachial artery undergoes eutrophic inward remodeling in the absence of hypertension or other hemodynamic changes. It has also been reported that alterations of the kallikrein-kinin system are associated with formation of aortic aneurysms. Conversely, after vascular injury, kinins mediate the beneficial effect of angiotensin-converting enzyme inhibitors that prevent neointima formation. These findings raise the intriguing possibility that decreased kallikrein-kinin system activity may play an important role in the pathogenesis of vascular remodeling and disease, while increased activity may have a beneficial effect.