As both the perforin/granzyme B-dependent granule exocytosis pathway[37-41] and the Fas signaling[42,43] have been implicated as potential mechanisms in oligodendrocyte and/or axonal injury and demyelination in MS, our findings taken together suggest that HGF might be effective in a potential therapeutic approach to reduce CTL effector function in CTL-mediated human autoimmune disorder of the CNS. The gene discussed is HGF; the disease is Autoimmunity.