Treatment of mice with TNF in combination with a global inhibitor of transcription such as d-galactosamine or actinomycin D induces lethal hepatitis.13 Another well-established mouse model of ALF consists of combined treatment with d-galactosamine and bacterial lipopolysaccharide (LPS), both inducing TNF expression and an acute inflammatory response that is predominantly directed toward the liver.14 The gene discussed is TNF; the disease is hepatitis A virus infection.