This has potential consequences as nuclear-cytoplasmic transport may be compromised with TDP43 shuttling and function particularly impaired as ALS patients carrying either G38R or D40G mutations have TDP43 pathology.7,15 The large nuclear sheathed Annexin A11 aggregates in motor cortex including prolific neuronal torpedoes from the G38R case suggest that cortical neurons may be more vulnerable to Annexin A11 dysfunction. Here, ANXA11 is linked to amyotrophic lateral sclerosis.