Importantly, Menke and colleagues reported recently that transformation of the human pancreatic carcinoma epithelial-like cell line PANC-1 with constitutively active Rac1(V12) profoundly altered the subcellular distribution of E-cadherin- β-catenin complexes and thereby epithelial cell-cell contacts in an IQGAP1-dependent manner, whereas cell transformation with dominant negative Rac1 (N17) had the opposite effect [141]. This evidence concerns the gene RAC1 and exocrine pancreatic carcinoma.