Statins (HMG-CoA reductase inhibitors) are widely used for the treatment of hypercholesterolemia. Statins reduce the risk of coronary pathology; they are well tolerated and have few adverse effects. During the last years mounting evidence suggest that statins could be also useful for several autoimmune and neurodegenerative diseases. Proposed mechanisms include effects on plasma lipoproteins, endothelial function, atheroma reduction, thrombosis and inflammation. The realization that brain ischemia produces inflammation of the brain opens a new field for discovery of novel therapeutic agents for stroke. Here, I comment on a paper from Chen et al. ("Statins induce angiogenesis, neurogenesis, and synaptogenesis after stroke", Ann Neurol 2003; 53: 743-751) that proposed that atorvastatin and simvastatin reduced tissue damage and enhanced functional outcome when administered to rats 1 day after experimental stroke. Animals treated with statins showed increases in vascular endothelial growth factor, cyclic guanosine monophosphate, angiogenesis, cell proliferation and neurogenesis, and increase in synaptophysin. Although the authors concluded that atorvastatin induced brain plasticity and had neurorestorative activity, I think that significant additional experiments are required in order to sustain some of the mechanisms proposed by them. However, evidence on the effect of statins on experimental autoimmune encephalomyelitis and other inflammatory disease is also discussed here, because they cast light on alternative mechanisms that could be responsible for the better outcome of stroke animals treated with statins. Inflammation is attractive in therapeutic terms, considering its rapid initiation, its progression for several hours after stroke and its enormous contribution to brain damage