LRRK2 and Parkinson disease: Interestingly, overexpression of Rab1, 3a, and 8a, which we (this study) and others [29] suggest as LRRK2 substrates, could rescue α-synuclein-induced cytotoxicity in cell and animal model of PD [54, 55], implying that Rab GTPases might be involved in multiple pathways that play crucial roles in the pathogenesis of PD.