These findings potentially suggest that the ability of PQBP3/NOL7 to localize to the nucleolus was more robust than the sequestration effects of Atxn1, Htt, and AR, and that any potential functional impairment of PQBP3/NOL7, in SCA7, HD, or SBMA/KD would not be based on sequestration to inclusion bodies. The gene discussed is ATXN1; the disease is spinocerebellar ataxia 7.