The screen showed that polyQ expansion favors formation of a protein complex containing RBM17 (RNA-binding motif protein 17) and attenuates formation and function of a protein complex containing the HMG-box protein capicua (CIC), providing insight into molecular pathogenesis of SCA presumably representative for other polyglutamine diseases [81]. Here, RBM17 is linked to autosomal dominant cerebellar ataxia.