In addition to reduced infarct volumes and improved neurological scores at 24 and 72 h after middle cerebral artery occlusion (MCAO; a commonly used animal model for ischemic stroke), fingolimod showed a deactivation of caspase-3, a reduction of terminal deoxynucleotidyl transferase-mediated uridine 5′-triphosphate-biotin nick end-labeling (TUNEL-) positive neurons, an activation of RAC-alpha serine/threonine-protein kinase (Akt) and extracellular-regulated kinase (ERK), and a Bcl-2 up-regulation, delineating an anti-apoptotic effect in neurons [211]. The gene discussed is AKT1; the disease is ischemic stroke.