Planar cell rearrangements control epithelial tissue morphogenesis and cellular pattern formation. They lead to the formation of new junctions whose length and stability determine the cellular pattern of tissues. Here, we show that during Drosophila wing development the loss of the tumor suppressor PTEN disrupts cell rearrangements by preventing the lengthening of newly formed junctions that become unstable and keep on rearranging. We demonstrate that the failure to lengthen and to stabilize is caused by the lack of a decrease of Myosin II and Rho-kinase concentration at the newly formed junctions. This defect results in a heterogeneous cortical contractility at cell junctions that disrupts regular hexagonal pattern formation. By identifying PTEN as a specific regulator of junction lengthening and stability, our results uncover how a homogenous distribution of cortical contractility along the cell cortex is restored during cell rearrangement to control the formation of epithelial cellular pattern. Display omitted •PTEN controls homogeneity of cell junction contractility and hexagonal cell packing•Myosin II is enriched at newly formed adherens junctions (AJs)•PTEN reduces MyoII level at newly formed AJs, promoting lengthening and stability•Hexagonal cell packing requires restoration of homogenous cortical contractility Cell rearrangements control tissue morphogenesis and cellular pattern. Bardet et al. show that PTEN promotes the lengthening and stability of newly formed adherens junctions by reducing their myosin II level. These results uncover how a homogeneous cortical distribution of myosin II is restored during cell rearrangements to control tissue organization.