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]. The gene discussed is AKT1; the disease is myocardial infarction.