Thus, it is crucial to use various models of parkinsonism—including laboratory animals such as transgenic mice with an overexpression of a mutant form of human alpha-synuclein (A53T; A30P), toxin-induced models (6-hydroxydopamine (6-OHDA), MPTP, and reserpine), and knockout mice lines with a depletion of Parkin/Park genes (Pink-1, DJ-1, and synuclein family proteins)—in order to fully understand the mechanisms of PD pathogenesis. This evidence concerns the gene SNCG and Parkinson disease.