However, regardless of which vascular mechanisms underlie the apparent lack of haemodynamic changes, the increased stroke susceptibility following arterial occlusion in BK−/− mice, along with the aggravated cell death under IVI in hippocampal BK−/− slice cultures, suggest a primarily neuronal mechanism for the protective effect of BK channels limiting brain damage during ischemia. The gene discussed is KCNMA1; the disease is stroke disorder.