However, after a 5-year follow-up, these patients manifested no signs of parkinsonism at neurological examination and had very slow rates of nigrostriatal dysfunction progression, in comparison to patients with sporadic PD (a mean of 0.56% vs. 9–12% annual reduction in putamen F-DOPA uptake), suggesting that the probability of developing clinical parkinsonism by single PARK2 mutation carriers is very low [56]. This evidence concerns the gene PRKN and Parkinson disease.