ARBs block AT1 leading to the likely activation of AT2 receptors in the brain.29 AT1 activation increases oxidative stress, neuroinflammation, endothelial dysfunction, and reduced cerebral perfusion.30 AT2 activation produces anti-inflammatory effects that can be neuroprotective,31 including inhibition of cerebral ischemia.32 Previous studies report that ARBs can reduce cerebrovascular inflammation resulting in neuroprotective effects. The gene discussed is AGTR2; the disease is endothelial dysfunction.