Park et al. active regenerative capacity related to young healthy swines, as well as the NBCA, which has known to eventu- ally induce parenchymal hypertrophy (23). In this study, most of the stenoses were within the parenchymal tract, but TIPS stenoses have actually occurred in both hepatic veins and the parenchymal tracts in clinical practices. This may be explained that the main cause of TIPS stenoses in this study was PIH within the hepatic parenchymal tract, and there was neither thrombo- sis nor intimal hyperplasia within the vascular sites. Our study has several limitations. First, the small and uneven sample sizes of the control and irradiated groups and short term follow-up period make it somewhat difficult to conclude the value of 166Ho in TIPS. The two weeks follow-up period is not sufficient to induce cirrhotic changes following the portal hypertension induced by NBCA embolization, even though the portal hypertension was sustained during the experimental period. Second, the concrete evidence for the persistence of portal venous hypertension was not sufficient. In our study, we found that the follow-up portography demonstrated the reconsti- tution of portal flow within the occluded portal vein in one branch of five pigs. However, active evaluation of the distal branches and collaterals was not performed. Liver function tests, histologic confirmation of the parenchymal tissue and long term follow-up of portal venous pressure are needed to confirm the successful creation of chronic portal venous hypertension in further studies. Third, compared with the human cirrhotic liver, our animal model still has a parenchymal difference such as periportal fibrosis, although the artificial induction of portal hypertension by embolic materials was done to mimic the hemodynamic situation of cirrhosis. This may be followed by the differences of response to radiation, biologic interaction of repair and regeneration, and the stenosis rates. 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