TARDBP and amyotrophic lateral sclerosis: Emerging evidence from cell culture and mouse experiments reveals that EV infection produces hallmark cellular and molecular phenotypes of ALS, including RNA-processing defects, impaired nucleocytoplasmic transport, neuroinflammation, compromised protein quality control, and most strikingly, TDP-43 (transactive response DNA binding protein-43) pathology, supporting a potential link between EV infection and ALS pathogenesis (Figure 1).