In a study by Scrocchi et al. (73), a defective glucose-stimulated insulin secretion was noted in mice which were deprived of the GLP-1 receptor in β-cells (GLP-1R−/−), while in another murine model of diabetes, the administration of GLP-1R agonist exendin-4 attenuated translational downregulation of insulin and improved beta cell survival (74). Here, INS is linked to diabetes mellitus.