In order to study the regulation of E-cadherin by protein kinase B (PKB), wild type SMMC 7721 hepato-carcinoma cells and a Gag-PKB/SMMC 7721 cell line where PKB activity is markedly increased compared with control cells were used. Interestingly, increasing PKB activity via insulin stimulation or Gag-PKB transfection does not enhance the E-cadherin in the level of mRNA and that of protein by using Northern blot and Western blot analysis, but markedly drives E-cadherin protein to cell surface by using flow cytometry analysis and immunofluorescence analysis localization of E-cadherin, which resulted in the increase of cell aggregation and the inhibition of cell apoptosis mostly via E-cadherin. Therefore, new evidences that elevation of PKB activity could drive functional E-cadherin molecule to cell surface are provided.