Loss-of-function mutations in PRKN and/or PINK1 being responsible for around 15% (PRKN) and up to 4% (PINK1) of early-onset parkinsonism implies that the accumulation of damaged mitochondria precipitates the destruction of dopaminergic neurons via the stimulation of oxidative stress and inflammatory processes [11,16,18]. This evidence concerns the gene PINK1 and Parkinson disease.