Previous studies show that Cerebrolysin acts through multiple molecular pathways to enhance functional recovery following neurological diseases and injuries, including interactions with GluR1 and GABA RA/B receptors, regulation of intracellular signaling cascades (PI3K/Akt, NF-κB, JNK, and p38-MAPK), and alterations in molecular mediators relevant to trophic activity (NGF, BDNF, IGF-1), glucose transport (GLUT1), inflammation (TNF-α, IL-1β), and neurotransmission (cholinergic, glutamatergic, and GABAergic) [25,26,32,33,34]. This evidence concerns the gene AKT1 and nervous system disorder.