Imperiale et al[8] regarded HE as an immune inflammation mediated by CD8+ T cell, and Japanese researchers found that IgG4 concentration was elevated in serum and cerebrospinal fluid in HE patients.[9] Our patient underwent sufficient antithyroid treatment but still developed HE, which suggested that HE was based on autoimmune background, independent of the thyroid functional state. Here, CD8A is linked to hereditary elliptocytosis.