Nevertheless, the generally persisting tendencies of an earlier AAO in MJD patients carrying the C/C genotype for rs1801582 in PRKN exon 10, along with the significant results using the family factor-adjusted analysis of the combined cohort, gave us confidence to explore the functional ramifications of the variant in PRKN on the molecular pathology of MJD. This evidence concerns the gene PRKN and Spinocerebellar ataxia type 3.