The CAG expansions were either in the SCA2-parkinsonism or classic cerebellar SCA2, which, together with the reported genetic overlap [5] and without clinical heterogeneity or ALS phenotype modification [4], [5], [15], [19], [28] support our hypothesis of CAG expansion in ATXN2 being monogenic ALS cause (at least for longer intermediate CAG expansions). Here, ATXN2 is linked to Parkinson disease.