To gain further insights into the mechanisms by which GBA1 mutations increase the risk for PD and lead to the development of GBA1-assiciated parkinsonism, we crossbred GBA1 mice carrying D409H knock-in mutation with human A53T α-synuclein Tg mice exhibiting neurological abnormalities, accumulation of α-synuclein aggregates, increased ER stress, neuroinflammation, and shortened lifespan [5, 19]. The gene discussed is GBA1; the disease is Parkinsonism.