The finding that tolerogenic properties of the liver are at least partially responsible for the difficulties in generating a valid model for AIH are supported by another TCR-transgenic model that has been developed by Zierden et al. They found a spontaneous chronic liver inflammation in Alb-HA/CL4-TcR double transgenic mice that express the influenza virus hemagglutinin (HA) under the control of the albumin promoter in the liver as well as HA-specific TCR on the majority of CD8 T cells [103]. The gene discussed is ALB; the disease is autoimmune hepatitis.