A widely studied model of experimental hepatitis is that induced by concanavalin A. Though this model does not reflect accurately the pathological entity of AIH in humans, it has provided evidence that liver damage mainly occurs within a Th1 scenario, with the involvement of activated CD4+ T cells and release of the proinflammatory cytokines interferon gamma and tumour necrosis factor alpha against a specific genetic background. The gene discussed is IFNG; the disease is hepatitis A virus infection.