Activation of GLP-1 by DPP-4 inhibitors and GLP-1 analogs, limits myocardial infarct size (IS) and causes upregulation in intracellular cascades like protein kinases, Akt/P-Akt, and extracellular signal-regulated kinases (ERK1/2) with protective profile against ischemia-reperfusion injury [4]. Here, AKT1 is linked to ischemia reperfusion injury.