Microglial KCa3.1 potentiate the neuroinflammatory response induced by oligomeric amyloid-β and LPS treatment, while pharmacological blockade or gene deletion of KCa3.1 has beneficial effects in rodent models of ischemic stroke, AD, and multiple sclerosis, reducing inflammatory factors such as TNF-α and IFN-γ expression in the spinal cord or the brain tissue [14, 15]. The gene discussed is KCNN4; the disease is ischemic stroke.