Patients treated with BMT are extremely susceptible to infection with blood-borne viruses that can cause liver disease of variable clinical severity, from minimal biochemical changes to fulminant hepatic failure. Facing a patient with liver disfunction after BMT, one must bear in mind that more than one cause of liver disease, of viral and/or non-viral origin, may coexist. Moreover, besides the most important hepatotropic viruses, other agents, like herpesviruses (including CMV, adenoviruses, Epstein-Barr virus) may also be implicated, sometimes causing a life-threatening fulminant hepatitis, due to their cytopatic effect. Liver disease history and viral markers before transplant, together with the accurate assessment of the timing and type of clinical and biochemical deterioration are useful tools for a differential diagnosis. Liver biopsy, if taken in the early posttransplant period, is often difficult to interpret, while in case of liver disease occurring during immunosuppression tapering, histologic examination may discriminate between an exacerbation of viral hepatitis and an acute onset of chronic liver GVHD. While it seems that hepatitis G virus does not cause liver disease, the presence of hepatitis B virus (HBV) or hepatitis C virus (HCV) infection is a matter of concern for its consequences both early after BMT and for long-term survivors. Despite screening for blood and marrow donors for HBV and, more recently, for HCV markers, the rate of post-transplant infection (4% and 4-15% respectively, confirmed in prospective studies) with those viruses indicates that viral hepatitis still remains an important clinical problem in this setting, although the prognosis of chronic HCV and HBV infection appears more benign than expected, especially in children.