Of these monogenic PD forms, homozygous or compound heterozygous loss-of-function mutations in the PRKN (or PARK2) gene account for about 50% of autosomal recessive juvenile Parkinsonism (ARJP) (OMIM: 600116 [https://www.omim.org/entry/600116]) cases and 77% of familial early onset Parkinson’s disease, starting at an age younger than 30 years2,3. This evidence concerns the gene PRKN and Parkinson disease.