Since then, other numerous genetic alterations in SNCA (single-point mutations, duplications, and/or triplication) [39,40,41,42,43,44,45] and other genes (GBA, PINK1, LRRK2, Parkin, or DJ1, among others) [46,47,48,49] gradually appeared as risk factors of PD early onset and progression, opening up possibilities for the development of genetic models that recapitulate the molecular origin the disease better than the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) or 6-hydroxydopamine (6-OHDA) neurotoxin ones do [50]. This evidence concerns the gene SNCA and Parkinson disease.