Of course, differences in CAG-length dependent pathology between HD and SCA3 may also be mediated by differences in the protein context of the polyglutamine domain between HTT and ATXN3, which may be further modulated by CAG-length (in-)dependent effects on HTT and ATXN3 splicing (Bettencourt et al. 2009; Harris et al. 2010; Sathasivam et al. 2013; Weishäupl et al. 2019; Hoschek et al. 2024). The gene discussed is ATXN3; the disease is Huntington disease.