Whereas the meningeal TLS observed in multiple sclerosis are proposed to mediate intrathecal somatic hypermutation and CSF-compartmentalized progressive disease (26), the absence of such structures in patients with LGI1 and CASPR2 antibody encephalitis, including one with a long untreated history, may explain their more monophasic course without progression. The gene discussed is LGI1; the disease is multiple sclerosis.