Previous studies have indicated that ALS-associated TDP-43 mutations or TDP-43 proteinopathy associated with non-familial ALS cause mis-splicing of STMN2 gene transcripts, splicing in a cryptic exon that results in greatly diminished steady-state levels of stathmin-2 mRNA and protein (Melamed et al., 2019). The gene discussed is STMN2; the disease is amyotrophic lateral sclerosis.