Using rat insulinoma INS-1 832/3 cells engineered by clustered regularly interspaced short palindromic repeat (CRISPR)/CRISPR-associated 9 (Cas9) to delete endogenous GLP-1R [40] stably expressing human SNAP-GLP-1R (INS-1 832/3 GLP-1R−/− SNAP-GLP-1R cells), we detected a rapid increase in TR-FRET with exendin-4, which reached a maximum within 10 min (Fig 1D). This evidence concerns the gene GLP1R and pancreatic insulinoma.