Researchers report that hypusination of the translation factor eIF5A regulates local protein synthesis in axons and mitigates pathology in models of FUS‑linked amyotrophic lateral sclerosis (ALS), according to a study in Nature Neuroscience. The team demonstrated that modifying eIF5A activity restores axonal translation defects caused by FUS mutations and improves cellular phenotypes associated with neurodegeneration. The work identifies a biochemical node—post‑translational hypusination of eIF5A—that can be pharmacologically targeted to normalize local protein production in neurons. Hypusination is a rare modification that activates eIF5A to promote translation elongation; here it links a specific molecular event to axon biology and FUS‑ALS pathology. The study positions eIF5A hypusination as a candidate mechanism for therapeutic development and follow‑up preclinical work.