The localized brain RAS activation is associated with neuroinflammation and neuropathy as demonstrated by the facts that central administration of Ang II, the major prohypertensive ligand of AT1 receptor, induces neuroinflammation and oxidative stress in vivo and in vitro (Bild et al., 2013; Bali and Jaggi, 2016; Abdul-Muneer et al., 2018), and AT1 receptor blockade ameliorates inflammation and improves brain function in animal models of epilepsy, brain ischemia and neurodegeneration (Saavedra et al., 2011; Tchekalarova et al., 2015; Valenzuela et al., 2016). This evidence concerns the gene AGT and epilepsy.