Indeed, this dysregulation could be mediated through either or both the sense CAG RNAs and antisense CUG RNAs, the latter of which is already supported by studies in SCA816 and SCA2.17 However, other studies focusing on SCA3 and Huntington’s disease suggest that CAG expansion RNAs may play a role in alternative splicing dysregulation.21 This evidence concerns the gene ATXN2 and juvenile Huntington disease.