In addition to potentially taming the T cell–mediated neural injury that underlies progression in MS (5), pharmacological inhibition of the PPP may be a powerful direct approach or adjunct therapy in patients with rapidly progressive immune-mediated neurodegenerative diseases mediated by autoimmune CD8+ T cells (69), including anti-GAD encephalitis and the paraneoplastic encephalitides involving autoimmune responses against targets such as KLHL11 (70), Hu, Yo, and Ma/Ta (71, 72). This evidence concerns the gene KLHL11 and neurodegenerative disease.