This assumption is supported by findings that the administration of lithium, which rescues the Wnt signaling pathway by inhibiting glycogen synthase kinase-3β, was neuroprotective against Dkk-1-induced neurotoxicity [21] and that striatal overexpression of siRNA of beta-catenin, the downstream component of Wnt signaling, caused an enlarged stroke volume [23]. Here, CTNNB1 is linked to stroke disorder.