Regarding the family of polyglutamine disorders, which includes Huntington’s disease, spinobulbar muscular atrophy, dentatorubral pallidoluysian atrophy, and spinocerebellar ataxia (SCA) type 1, 2, 3, 6, 7 & 17 [1], [2], [3], [4], a gene duplication of ataxin-1-like (ATXN1L)/Brother of ataxin-1 (Boat), the respective paralog of the disease-causing protein ataxin-1 (ATXN1), ameliorated the observed neurotoxicity in a SCA1 mouse model, indicating overlapping functionality between paralog and disease protein [5]. This evidence concerns the gene ATXN1L and juvenile Huntington disease.