Intermediate-length CAG expansions in ATXN2 can lead to atypical SCA2 phenotype [8]–[10], however their association with ALS phenotype featured by shorter survival and onset at ∼54years of age helps to avoid misdiagnosis of ALS as SCA2 with motor neuron disease [29]. This evidence concerns the gene ATXN2 and amyotrophic lateral sclerosis.