Similar experiments were performed in BULB/c mice homozygous for the knocked-out TGF-β1 allele (TGF-β1−/−), with the difference that these mice developed spontaneous AIH, in contrast to mice with overexpression of the dominant-negative TβRII receptor, in which AIH requires prior immunization. The gene discussed is TGFB1; the disease is autoimmune hepatitis.