In this study, we explored the role of BK channels in microglial phagocytosis after tMCAO and demonstrated that activation of BK channels during the first 3 days after tMCAO promoted microglial phagocytosis and alleviated neurological deficit after ischemic stroke; ERK was involved in the activation of BK channel-mediated microglial phagocytosis. The gene discussed is MAPK1; the disease is ischemic stroke.