The central role of alpha-synuclein accumulation in the pathology of Parkinson-GBA1 was further highlighted by the reciprocal relationship between GCase activity and alpha-synuclein; demonstrated in SH-SY5Y cell cultures, neuronal cultures, conduritol-β-epoxide (CBE)-treated mice and transgenic Gba1 mouse models (Manning-Boĝ et al., 2009; Cullen et al., 2011; Mazzulli et al., 2011; Sidransky and Lopez, 2012; Cleeter et al., 2013; Osellame et al., 2013; Sardi et al., 2013; Schöndorf et al., 2014; Xu et al., 2014; Yang et al., 2017). The gene discussed is GBA1; the disease is Parkinson disease.