Currently, eight central players are considered to be involved in T2DM pathophysiology—the ominous octet—composed by muscle/liver insulin resistance, β-cell failure, enhanced lipolysis, hyperglucagonaemia, dysregulation of hepatic glucose production, brain insulin resistance, increased renal glucose reabsorption, and incretin hormone [glucagon-like peptide 1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP)] deficiency, all contributing to a persistent state of hyperglycaemia [6]. Here, GLP1R is linked to type 2 diabetes mellitus.