Researchers at the La Jolla Institute for Immunology and Columbia University Irving Medical Center have uncovered compelling evidence suggesting that amyotrophic lateral sclerosis (ALS) may be driven by autoimmune responses. The study revealed that CD4+ T cells from ALS patients aberrantly target the neuronal protein C9orf72, a hallmark protein implicated in ALS pathology. This self-directed immune attack likely contributes to rapid disease progression and points toward novel immunomodulatory treatment strategies. These findings disrupt traditional views of ALS etiology and open new avenues for precision interventions targeting autoimmune pathways.