In human medicine, the role of autoantibody-mediated encephalitis has profoundly changed the assessment of neurological diseases, and new underlying autoantibodies are continuously being discovered, the most common of which are antibodies against the N-Methyl-D-aspartate (NMDA) receptor and the synaptic protein leucine-rich glioma inactivated-1 (LGI1) (1). This evidence concerns the gene LGI1 and encephalitis.