Endothelium-derived nitric oxide (eNO) is a central regulator of vascular function and blood flow. eNO is a potent vasodilator, inhibits platelet aggregation and prevents monocytes adhesion. In addition, NO availability is an important determinant of the functional capacity of endothelial progenitor cells and neovascularization. Consequently, eNO plays a central protective role during the pathogenesis of ischaemic stroke. Experimental and clinical studies have demonstrated that statins increase the bio- availability of endothelial NO indirectly via cholesterol-lowering as well as through direct cholesterol-independent mechanisms. On the basis of animal studies and clinical trials, statins have emerged as a potential novel strategy to protect from ischaemic strokes. These data raise the questions whether patients with acute cerebral ischaemia may benefit from intravenous treatment with a statin and, whether these patients are at risk when their ongoing statin treatment is withdrawn.