In a previous study, deletion of the PARK16 locus gene RAB7L1 in primary rodent neurons, or loss of its ortholog in Drosophila dopaminergic neurons, resulted in degeneration similar to that observed with expression of a familial PD mutant form of LRRK2, while Rab7L1 overexpression rescued this mutant phenotype [209]. The gene discussed is RAB29; the disease is Parkinson disease.