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Full list of author information is available at the end of the articleBackground Subarachnoid hemorrhage (SAH) caused by saccular intracranial aneurysm (sIA) rupture is a rather common disease with a high fatality and morbidity. The incidence of aneurysmal SAH is 10–11 per 100 000 in North America and Europe, and twice as high in Finland and Japan [1]. Almost half of aneurysmal SAH patients die and half of survivors are left disabled [1,2]. Main risk factors for aneurysmal SAH are smoking, hypertension, female gender, familial background, and alcohol, caffeine, or cocaine abuse [2-4]. How these risk factors affect the sIA wall and trigger rupture, remains unknown. Formation of an intracranial aneurysm does not always lead to eventual aneurysm rupture, and formation of a sIA seems to be a separate process from sIA rupture [5]. Knowledge of the pathobiology that leads to the degen-eration of an existing sIA wall into a rupture-prone sIA, is necessary to identify sIAs at risk of rupture, and in order to develop novel therapies that would reduce th