Immunopathological mechanisms in amyotrophic lateral sclerosis (ALS) include various processes, such as the phagocytosis of apoptotic and nonapoptotic neuronal cells by inflammatory macrophages, cytotoxic effects mediated by granzyme-positive CD8+ T cells, disruption of the blood‒brain barrier by Th17 cells, and IL-6 trans-signaling, which has been shown to exert dose-related toxicity in mouse brains. The gene discussed is CD8A; the disease is amyotrophic lateral sclerosis.