Activation of Akt1 is usually cytoprotective, such as its function during endothelial cell hypoxia (Somanath, Razorenova, Chen, & Byzova, 2006), and Akt1 has been extensively studied and is considered to be neuroprotective in stroke (Zhao, Sapolsky, & Steinberg, 2006), with Akt1 and Akt3 proteins degrading as early as 1 hr after stroke (Xie et al., 2013). This evidence concerns the gene AKT3 and stroke disorder.