The answer to the question posed in this title is “yes”, but affirmation is highly qualified. (1) Stroke is not a homogeneous clinical disease state but a dynamic process whose etiologies are manifold. Its causes vary from the commonplace atherothrombotic occlusion of brain arteries and emboli of cardiac origin to rare and complex precipitants. (2) Stroke is not a hemogenous pathologic state. Parenchymal hemorrhage, hemorrhagic infarctions and bland infarctions are very different forms of brain destruction with differing outcomes. The great triumvirate of risk factors in stroke are advanced age, arterial hypertension and heart disease. All of these conditions tend to coexist with the process of atherosclerosis. Hypertension and cardiac disease are potentially amenable to early diagnosis and treatment. In clinical studies, the effective treatment of arterial hypertension is emerging as the clearest evidence that risk factor modification is correllated with a decline in stroke. Therapy for some cardiac diseases constitutes effective stroke prevention as well. Other less direct risk factors for stroke tend to parallel the severity and extent of the atherosclerotic process. These include diabetes mellitus, hyperlipidemias and obesity. Therapeutic modification of these factors has debatable influence on the incidence of stroke and may reflect the atherosclerotic process to medical intervention. Some clinical studies have suggested that certain antiplatelet agents postpone stroke and limit TIAs, at least in males. Anticoagulants may prevent TIAs but do not appear to prevent stroke. Surgery has a definable range of risks and clearly demonstrated benefits in properly selected patients in whom it may relieve TIAs and postpone a given stroke. Surgery does not alleviate an individual patient’s overall stroke risk. The process of stroke prevention will remain imperfect until therapies for hypertension and heart disease are accompanied by more effective treatment of atherosclerosis.