The molecular basis for increased neurogenesis and improved functional performance after the administration of Cerebrolysin was found in the modulation of the phosphatidylinositol-3-kinase (PI3)/AKT, glycogen synthase kinase 3 beta (GSK3β) and Sonic hedgehog (Shh) signaling pathways, the latter being currently discussed as a pivotal pathway in modulating blood-brain barrier integrity and neuroprotection post-stroke [5-7]. The gene discussed is GSK3B; the disease is Stroke.