The pathogenic cascade leading to αSyn aggregation and the neurodegeneration of this oligodendroglioneuronal proteinopathy is poorly understood [10,11], but recent studies elucidated the early cellular dysfunction in MSA indicating both increased susceptibility to oxidative stress and disease-related translocation of αSyn to the cell nucleus [12], while others demonstrated mislocalization of myelin-associated oligodendrocyte basic protein (MOBP) and huntingtin protein 1 (HIP1) due to DNA methylation interacting with αSyn in the oligodendrocyte as a pathogenic way of MSA [13]. This evidence concerns the gene HIP1 and multiple system atrophy.