Early rodent studies demonstrating GLP-1RA treatment expansion of the beta cell mass generated excitement about its potential to reverse T2D in humans.22 Subsequent work showed that GLP-1R-mediated stimulation of beta cell proliferation only occurred in young but not older rodents.33 In human subjects, while GLP-1RAs may improve beta cell function during treatment, there is no clinical evidence of sustained improvement after treatment discontinuation in either adults or adolescents.34–37. The gene discussed is GLP1R; the disease is type 2 diabetes mellitus.