Tumor formation is a complex process involving many cytological events, including unregulated cellular growth and disruptions to cellular adhesion. E-cadherin (E-cad), a prototypical member of cadherin family, acts as a molecular zipper to bind cells to tight adherens junctions, and its loss or disruption has been linked to epithelial tumorigenesis. The expression of Bcl-2—a cell-death regulator that confers a survival advantage on cells—has also been linked to various carcinomas. These two proteins may be biologically related, since Bcl-2 impacts on E-cad expression, but until now it was not clear what this relation meant. In the September 15 Journal of Cell Science, Laiji Li and colleagues at the University of Alberta show that Bcl-2 expression disrupts adherens junctions through its effects on E-cad expression, ultimately decreasing cadherin-mediated cell–cell adhesion (Journal of Cell Science, 116, 3687-3700, September 15, 2003).