Features of anti-LGI1 encephalitis suggesting a pathophysiological action of bivalent, i.e. IgG1/2/3, activity have been observed before: LGI1 antibodies were experimentally able to internalize LGI1-ADAM22/23 complexes, which is impossible for IgG4 [34, 35, 38, 45]; another study found that patients with FBDS and cognitive impairment had a higher proportion of LGI1-IgG1 antibodies compared to those with FBDS only (MRI data were not given) [45]. The gene discussed is ADAM22; the disease is viral encephalitis.