The general concept of the AIH immunopathophysiology is that loss of self-tolerance of autoreactive T cells results in T helper (TH) 1, TH2, and TH17 cells, accompanied by regulatory T cell aberrations (2, 7, 8), stimulating CD8 T cells, B cells and NK cells to ultimately damaging hepatocytes via cellular, humoral, and granzyme mediated auto-aggression, respectively (9). The gene discussed is CD8A; the disease is autoimmune hepatitis.