The well-documented beneficial effects of KCa3.1 blockers in models of ischemic stroke [29], traumatic brain injury [13], and atherosclerosis [47], which primarily seem to be mediated through inhibition of detrimental microglia/macrophage function, considerably add to KCa3.1′s attractiveness as a novel target for treating the dominant group of AD patients presenting with both degenerative and vascular pathologies. Here, KCNN4 is linked to Alzheimer disease.