Depletion of Akt3 markedly downregulated both E-cadherin and NCAM expression on protein as well as mRNA level in the K-Ras(V12)-overexpressing PANC-1 cells (Fig. 6), thus classifying Akt3 as a key mediator of oncogenic K-Ras-modulated cell-cell adhesion in pancreatic carcinoma cells. Here, AKT3 is linked to exocrine pancreatic carcinoma.