In toxin-induced PD mouse models, DA-JC1, a novel dual GLP-1/GIP receptor agonist, improved motor impairment, increased the number of dopaminergic neurons in the substantia nigra, enhanced BDNF levels, and modulated apoptosis signaling pathways by altering the expression of Bax and Bcl-2 [89, 90]. The gene discussed is GLP1R; the disease is Parkinson disease.