Background and Goals Liver failure from non-alcoholic fatty liver disease (NAFLD) is an increasing indicator for liver transplant and recurrence of fatty liver in transplanted grafts has been documented. of extra fat appeared as metastatic disease on PET imaging [2] but these reports are from native livers in individuals with known breast and colorectal malignancy respectively using an imaging modality not commonly used in the post-liver transplant setting. The first reports of recurrent NASH following liver transplantation were published in the late 1990s [3]. Since then the trend of post-transplant NASH is definitely common if not expected in certain populations. The major risk factors for developing recurrent or de novo NASH include components of the metabolic syndrome [4 5 and may be more widespread in post-transplant sufferers because of the usage of corticosteroids and calcineurin inhibitors [6]. Extra studies have discovered pre-transplant liver organ graft steatosis being a risk factor [7] also. Our affected individual had several risk elements including a BMI of 40 with significant putting on weight pursuing transplant difficult to regulate diabetes mellitus and the existing usage of tacrolimus aswell as the original usage of prednisone therapy pursuing his transplant. Provided the increased identification of disease recurrence and the chance factors involved research have now started to spotlight the implications of such results. Initial case research reported that steatosis can form within six months of transplant and cirrhosis within 24 months in sufferers that had been transplanted for NASH [4 8 9 A more recent retrospective review in 2009 2009 FLJ39827 concluded GDC-0980 that although recurrent fatty liver disease was seen in up to 70% of their post-transplant human population only 25% experienced recurrent NASH and none of these individuals had graft failure requiring re-transplantation at 3 years. This study also found that in the individuals with recurrent NASH over one-third experienced normal liver functions tests at the time of diagnosis [10]. Additional studies have estimated up to 50% of individuals have normal liver enzymes at the time of diagnosis [7]. In contrast another extended study of individuals transplanted for cryp-togenic cirrhosis or NASH saw a 10% incidence of bridging fibrosis or cirrhosis in the 10-yr time point mostly in individuals who developed recurrent NASH. However the recurrence of fatty liver disease with this patient human population did not significantly affect GDC-0980 survival compared to individuals who had additional indications for transplant in the control group. In fact individuals who have been transplanted for NASH or cryptogenic cirrhosis were more likely to pass away of cardiovascular disease than recurrent liver disease [11]. Additional studies have shown an increase in early mortality among individuals transplanted for NASH with survival equilibrating with additional indications for transplant at 3 years and beyond [12 13 inferring the reduced survival was a perioperative complication of cardiovascular disease rather than recurrent liver disease. In a recent study Dumortier et al. examined the development of de novo NASH in individuals transplanted for additional indications primarily alcoholic and HCV-related cirrhosis. It was found that even with this patient human population excluding patients with recurrence of their primary disease 31 of patients developed steatosis and 3.8% developed GDC-0980 NASH [7]. Based on these patients with significant risk factors for fatty liver disease pre-transplant can have these factors exacerbated after transplantation because of the required immunosuppressive regimens; therefore considerations need to be made in the management of these patients post-transplant. As the transplant community continues to grapple with metabolic syndrome care it is important to catalogue the atypical presentations of the increasingly common NAFLD developing in transplanted livers. Detection of a new liver mass in a post-transplant patient should always raise concerns for malignancy or infection. However it is important to remember that uneven or focal fatty infiltration is also possible particularly in patients with risk factors for recurrent fatty liver disease. Awareness of this entity can prevent unnecessary and invasive testing. Acknowledgments This extensive research was supported in part a grant.