In both diabetic and non-diabetic rodent models of cerebral ischemia, exenatide, lixisenatide, semaglutide, and liraglutide increased the expression of the anti-apoptotic factor B-cell lymphoma 2 (Bcl-2) and decreased the expression of the pro-apoptotic factor Bcl-2-associated X protein (Bax), consequently leading to a reduced Bax/Bcl-2 ratio and reduced apoptosis, possibly through ROS reduction and activation of the PI3K/Akt and MAPK pathways [73, 86, 87, 92, 93]. Here, AKT1 is linked to brain ischemia.