The observation that deficits of Kir4.1 channels in NG2-glia contribute to the loss of myelin in tMCAO highlights a new role of NG2-glia in physiological/pathological conditions in the brain and sheds light on a potential therapeutic target of NG2-expressing Kir4.1 channels for the treatment of ischemic stroke. The gene discussed is KCNJ10; the disease is ischemic stroke.