Additionally, one can hypothesize that AR gene expansions may, in themselves, confer an increased risk of ALS—analogous to associations previously reported for intermediate CAG repeat expansions in two other genes, ATXN2 [40] and HTT [41], except that larger expansions in these genes are primarily associated with other phenotypes (SCA2 and Huntington’s disease, respectively). This evidence concerns the gene ATXN2 and juvenile Huntington disease.