Specifically, immunofluorescence showed consistent colocalization of these NMDAR subunits with IgG, supporting the notion that dysmorphic neurons with coexpression of NR1/NR2A/NR2B and IgG in OT play a significant role in the pathogenesis of anti-NMDAR encephalitis (25, 54). The gene discussed is GRIN1; the disease is encephalitis.