Genetic analysis of Hungarian EOPD patients revealed mutations affecting several genes with varying degree of association, such as DNAJC6, DNAJC13, EIF4G1, GBA, LRRK2, PRKN, PINK1, PLA2G6, SNCA, and SYNJ1. Studying the functions of their protein products further elucidate the potential role and interplay in the pathomechanism of neurodegeneration, like mitochondrial dysfunctions and impaired autophagy-based protein or organelle degradation pathways, which indeed can lead to development of PD (Ryan et al., 2015). Here, PRKN is linked to Parkinson disease.