Cortical actin and adherens junctions are the two main factors that define cell shape in epithelial cells by modifying contractility and cortical tension at the cell surface. These contractile forces and adhesion work in an integrated manner to determine epithelial cell shape. In this study, Joshua Greig and Natalia Bulgakova (Greig and Bulgakova, 2020) address the interplay between cortical actin and E-cadherin (E-cad; encoded by the shotgun gene in Drosophila)-mediated adhesion in regulating cell shape in vivo. By making use of the elongated anisotropic cells of the Drosophila embryonic epithelium, the authors show that p120-catenin (p120ctn), a known regulator of E-cad, interferes with cell elongation by modulating the opposing activity of two different small GTPases. p120ctn activates RhoA (Rho1 in flies) specifically at the cell borders that are orthogonal to the anterior–posterior embryonic axis (AP borders) and are under high tension. This inhibits cell elongation by increasing cortical actomyosin and inhibiting clathrin-mediated endocytosis of E-cad. Conversely, p120ctn also recruits the GTPase Arf1 to the membrane where it promotes E-cad endocytosis, leading to cell elongation. Moreover, RhoA and Arf1 are also interconnected, and their opposing activities are resolved locally at AP borders, where RhoA inhibits Arf1. Thus, this study shows that p120ctn is responsible for the regulation of cell adhesion, by establishing a dynamic interplay between the actomyosin cortex and the endocytic machinery that ultimately controls cell shape.