Studies focusing on toxin-induced PD models (paraquat [2,3], rotenone, 6-hydroxydopamin (6-OHDA), 1-methyl-4-phenylpyridinium iodide (MPP+) [4]) as well as on genetic PD cases (LRRK2 [5,6], PTEN-induced putative kinase 1 (PINK1) [7,8], DJ1, α-synuclein (SNCA)) point out that, at first glance, cell death in PD appears to be related to mitochondrial dysfunction, reactive oxygen species (ROS) generation, cytochrome c release, activation of mitogen-activated protein kinase (MAPK) pathways, autophagy impairment, and/or disruption of calcium homeostasis. This evidence concerns the gene CYCS and Parkinson disease.