Ubiquitin-mediated proteasome degradation has also been proposed as a mechanisms for degradation of transmembrane proteins (VE-Cadherin, Claudin-5 and Occludin) and intracellular adaptors (ZO-1 and β-catenin) that anchor transmembrane junctional proteins to the cytoskeleton in various diseases including ischemic stroke (reviewed in [20, 21]). This evidence concerns the gene CLDN5 and ischemic stroke.