In particular the neuropathological evaluation of brains from GD patients with parkinsonism and PD subjects who carry GBA1 mutations along with studies in animal models of GD disease, neuronal cultures with deficient GCase activity, human iPSC neurons derived from GBA1 mutation carriers, as well as induced pluripotent stem cell (iPSC)-derived neurons from GD and PD individuals carrying GBA1 mutations, have revealed the presence of a-Syn aggregates or accumulation [17, 20–23]. This evidence concerns the gene GBA1 and Parkinsonism.