STMN2 and amyotrophic lateral sclerosis: Indeed, reduced STMN2 expression associated with the presence of the non-functional, truncated STMN2 was reported both in in vitro 2D models depleted of TDP-43 and in post-mortem brain and spinal cord tissues of familial and sporadic ALS patients with underlying TDP-43 pathology, including ALS patients with Chromosome 9 Open Reading Frame 72 (C9Orf72) repeat expansions, the most common genetic cause of ALS [8].