A current theory on the pathogenesis of SCA1 is that polyglutamine expansion disrupts the physiological interaction between ATXN1 and nuclear proteins regulating gene transcription and RNA processing, such as Capicua, retinoic acid orphan receptor-α (RORα), and RBM17 [4]. This evidence concerns the gene ATXN1 and spinocerebellar ataxia type 1.