Stathmin-2 (STMN2) is a target of the ALS-protein TDP-43 suggesting that loss of STMN2 due to TDP-43 pathology could contribute to the development of ALS. However, no studies in animals had tested the function of STMN2. Kelsey Krus, an MD/PhD student in the lab, made a STMN2 mouse model and discovered that even modest reductions in STMN2 induces a slowly progressive disruption to neuromuscular junctions leading to motor function defects, two key hallmarks of ALS. Hence, Kelsey’s findings support the hypothesis that STMN2 reduction due to TDP-43 pathology contributes to ALS pathogenesis, and provides a strong rationale for clinical trials to restore STMN2 expression in ALS patients.