Several studies have posited that TCF7L2, a significant gene implicated in the etiology of type 2 diabetes mellitus (T2DM), could potentially disrupt GLP1, diminish the expression of GLP1R and glucose-dependent insulinotropic polypeptide/gastrointestinal inhibitory peptide (GIP) receptor (GIP-R) and impede β-cell function through the stimulation of insulin secretion (in concert with GIP). This evidence concerns the gene GIPR and diabetes mellitus.