The Parkinson's variant or MSA‐P is characterized by striatonigral degeneration (SND), whereas the cerebellar variant or MSA‐C reflects olivopontocerebellar atrophy (OPCA).1 The PLP‐hαSyn transgenic mouse model recapitulates most of the clinical and pathophysiological features of MSA by overexpressing human α‐syn under the oligodendrocyte PLP (myelin proteolipid protein) promoter, which leads to GCI formation, microglial activation, and selective neurodegeneration.6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 16. This evidence concerns the gene PLP1 and striatonigral degeneration.