Moreover, Bede et al. (2021) revealed that the observation of cerebellar abnormalities in a large population of ALS patients, genotyped for carrying intermediate-length repeat expansions in ATXN2 or hexanucleotide repeat expansions in C9orf72, was not driven by the detection of intermediate-length alleles of ATXN2, showing cerebellar atrophy (involving the posterior lobes and the vermis) in the group carrying repeat expansions in C9orf72 and a predominantly anterior lobar pathology in sporadic ALS patients. Here, ATXN2 is linked to Cerebellar atrophy.