Since the recognition of autoimmune limbic encephalitis (ALE) in the mid-2000s, such as anti-N-methyl-D-aspartate receptor (NMDAR) and leucine-rich glioma-inactivated 1 (LGI1) encephalitis [4], the existence of HE has become more questionable [5]. This evidence concerns the gene LGI1 and viral encephalitis.