One promising target to control microglia phenotype is the Ca2+-activated K+ channel (KCa3.1), which is involved in microglia activation in different pathological conditions such as glioma,14 spinal cord injury,15 ischemia16 and Alzheimer's Disease.17 In particular, KCa3.1 blockade reduced infarct area and glioma invasiveness in rodent models of cerebral ischemia and cerebral tumor14, 16 and reduced the neurotoxicity of microglia upon lipopolysaccharide (LPS) or oligomeric amyloid β exposure.18, 19 Interestingly, KCa3.1 expression level negatively correlates with patient prognosis.20 This evidence concerns the gene KCNN4 and Alzheimer disease.