Together with a striking amount of recent genetic data linking PD risk to genes involved in endolysosomal functions, including β-glucocerebrosidase (Aharon-Peretz et al., 2004; Gan-Or et al., 2008), ATP13A2 (Ramirez et al., 2006), VPS35 (Vilariño-Güell et al., 2011; Zimprich et al., 2011) and RAB7L1 (Gan-Or et al., 2012), our data establishes dysfunction of the endolysosomal pathway as a central pathogenic mechanism in PD. This evidence concerns the gene ATP13A2 and Parkinson disease.