Thus, all currently available data indicate that reduced RAB8A protein levels and/or altered RAB8A phosphorylation/activation correlate with various cellular alterations related to PD pathogenesis, and our study demonstrates for the first time a novel role for a pathogenic LRRK2-mediated inactivation of RAB8A that impairs endolysosomal trafficking and correlates with a decrease in RAB7A activity. This evidence concerns the gene RAB7A and Parkinson disease.