Under ischemic conditions, CaMKKβ/2 exhibits protective roles in the endothelial cells and blood–brain barrier through SIRT1 phosphorylation and activation [145], consistent with a report showing that the genetic deletion of CaMKKβ/2 in female mice exacerbated ischemic injury and increased hemorrhagic transformation after stroke [146]. This evidence concerns the gene CAMKK2 and Stroke.