Intermediate size ATXN2 expansions comprise a risk factor for ALS through mRNA-mediated TDP-43 interaction [27, 35–37], while larger polyglutamine expansions in ATXN2 lead to Levodopa-responsive Parkinsonism [38] or to prominent cerebellar involvement with later progression to a multisystem atrophy of the nervous system, known as spinocerebellar ataxia type 2 (SCA2) [39]. This evidence concerns the gene ATXN2 and Parkinson disease.