GLP-1R-mediated stimulation of PI3K/Akt promotes cell survival through inhibition of pro-apoptotic proteins, upregulation of Bcl-2, stabilisation of mitochondrial membranes, and activation of PGC-1α-dependent mitochondrial biogenesis, effects first demonstrated in neuronal cultures by Li et al. and subsequently confirmed in multiple toxin-based PD models [9,41,57,79,86]. The gene discussed is GLP1R; the disease is Parkinson disease.