HIPK2 and cerebellar ataxia: We speculate that such overexpression is probably because of a severe proteasomal dysfunction that inhibits β-catenin degradation, a phenomenon typically linked to neurodegenerative disorders10, 21 such as Parkinson's disease22 and spinocerebellar ataxia.23 Therefore, we hypothesize that β-catenin is ubiquitinated but not degraded in Hipk2−/− Purkinje cells.