Experiments with primary fibroblast cultures from PD patients deficient of functional Parkin and in cells overexpressing the Rab7K38R mutant that cannot be ubiquitinated demonstrated that in these situations, the Rab7 capacity of binding to its effector molecule Rab7-Interacting Lysosomal Protein (RILP) is diminished [32]. This evidence concerns the gene PRKN and Parkinson disease.