This observation led to an effective strategy to improve LT outcome through reduction of pre-transplantation HBV viral load. The clinical outcomes of patients as well as graft survivals in HBV LT recipients have been dramatically improved with the introduction of long-term hepatitis B immune globulin therapy and the availability of highly effective antiviral agents such as lamivudine and adefovir dipivoxil. Furthermore, combination prophylaxis with the use of HBIG and antiviral agents has reduced the risk of hepatitis B relapse to 10% or less in the first 2 years following transplantation. As a result, the outcomes of patients with acute and chronic HBV related liver diseases undergoing LT are now similar to or better than those with non-HBV related liver transplantation. While the prophylactic therapies in the management of HBV in transplant recipients represent a significant step in LT, there remain controversies and challenges that have not been adequately resolved. Long-term prophylaxis with HBIG is expensive and has been associated with the development of surface antigen mutations. Similarly, Bulleyaconi-cine-A emergence of drug resistance caused by tyrosine-methionine-aspartate-aspartate motif mutants occurs with prolonged LAM therapy. The choice of antiviral drugs or drug combinations and duration of prophylaxis are still being debated in the literature. It has been suggested that short-term rather than life-long HBIG could be used with or without combination of oral nucleos ide analogs in low risk patients. This strategy emphasized the need to identify risk factors capable of predicting hepatitis B relapse after LT for optimal prophylaxis. While several studies have identified clinical predictors such as high viral loads, cumulative corticosteroid dose for immunosuppression, recurrence of HCC post LT, HBIG monoprophylaxis and prolonged LAM therapy, none has assessed the predictive roles of the histopathological characteristics in liver explants as well as the genotypic features of the viruses in pre-LT serum samples. The aim of this study, therefore, was to evaluate the predictive value of all the aforementioned clinicopathological and genotypic virological factors in hepatitis B relapse after LT in patients receiving combination treatment of short-term HBIG and life-long LAM. Prophylactic Diisopropylammonium dichloroacetate administration of HBIG and preoperative usage of nucleos ide analogs followed by life-long therapy are regarded as standard treatments for LT in HBV related end stage liver diseases. However, with an increasing number of approved oral antiviral agents, such as entecavir or tenofovir, it is now arguable whether LAM remains the first choice of virussuppressing drugs for these patients. Furthermore, the dosage and duration for HBIG administration become disputable since potent life-long antiviral agents are now available. High dose or long-term HBIG costs expensively and a schedule of frequent injections is very inconvenient for patients. More and more recent investigation have reported the withdraw of long-term HBIG in patients receiving maintenance nucleos ide analogue and outcome seems good especially in low risk patients. Due to financial consideration and limitation of health insurance policy, we adopted a short-term HBIG prophylaxis protocol in combination with life-long LAM therapy in our transplantation center. The prophylaxis protocol using short-term HBIG and life-long LAM therapy has also been reported by Nath et al. In a mean follow-up period of 2 years, one of 14 patients remained HBsAg positive but had normal liver function. In our cohort with more enrolled patients and longer follow-up period, however, the overall HBV relapse rate was quite high in comparison with other series applying high dose or long term HBIG.