In addition, as observed in vitro[6], our results indicate that infected hepatocytes are directly killed by the antigen- specific T cells and not by a bystander effect through continuous secretion of IFN-γ or other lymphokines by the injected T-cell clones or host vs graft immune response since concomitant infection of TAP-deficient mice does not lead to protection after treatment with the CS specific T-cell clone and/or naïve BALB/c hepatocytes. The gene discussed is IFNG; the disease is infection.