Although it is possible that the α-synuclein aggregates used in our study do not precisely recapitulate the ability of toxic α-synuclein species to mediate vesicle rupture in PD, a number of other in vitro and in vivo studies collectively suggest lysosomal dysfunction may be a central aspect of PD pathology (reviewed in [39]). The gene discussed is SNCA; the disease is Parkinson disease.