Currently, targets of antidiabetic drugs address several separate elements in the β-cell that potentially converge on TCF7L2 function.43 Direct or indirect stimulation of GLP-1 activity via treatment with DPP-4 inhibitors, GLP-1R agonists, or GPR119 agonists leads to activation of β-catenin via increased cAMP levels and improved TCF7L2-driven β-cell function.43 TCF7L2 could be appreciated as a new target for diabetes treatments. The gene discussed is GPR119; the disease is diabetes mellitus.