Over 40 mutations in TARDBP have been identified in ALS patients; moreover, aggregation and loss of nuclear TDP-43 are the pathological hallmarks of the vast majority of ALS cases [41], suggesting that TDP-43 dysfunction and the subsequent, altered processing of STMN2 could be a hallmark of ALS pathology. Here, STMN2 is linked to amyotrophic lateral sclerosis.