Polyglutamine protein TBP binds to the TATA-box of gene promoters to trigger transcription, but when the polyglutamine tract is expanded, in spinocerebellar ataxia type 17 (SCA17), changes its phase separation capacity and probably its ability to co-condense with transcription co-activators (Figure 2), leading to transcriptional dysregulation, a mechanism implicated in many polyglutamine diseases [1,3,67,70]. Here, TBP is linked to spinocerebellar ataxia type 17.