Rab12-mediated accumulation and activation of LRRK2 on lysosomes during lysosomal damage were enhanced in PD-associated mutants of LRRK2 or even VPS35, even under non-damaged conditions, but were not enhanced beyond wild-type during damage [54], suggestive of a Rab12-dependent lysosomal response mechanism that might be constantly activated in the course of PD pathogenesis with these mutations. This evidence concerns the gene VPS35 and Parkinson disease.