Specifically, major histocompatibility complex I (MHCI) depletion in resident microglia or the lack of CD8+ T cell infiltration in the spinal cord of β2 microglobulin-deficient hSOD1G93A mice (which express little if any MHCI on the cell surface and are defective for CD8+ T cells) delayed motor symptoms and prolonged the survival mean time, suggesting that microglia interact with infiltrated CD8+ T cells through MHC complex, promoting MN death in ALS. The gene discussed is CD8A; the disease is amyotrophic lateral sclerosis.