Having described the functions of parkin in the modulation of α-synuclein accumulation, PTM-mediated aggregation, and attenuation of α-synuclein-mediated toxicity, we hypothesize that α-synuclein aggregation leading to the formation of intracellular micro-aggregates might be an underlying intracellular pathogenic mechanism in PARK2-related PD that is more common than the formation of Lewy bodies. This evidence concerns the gene PRKN and Parkinson disease.