During neocortical development, the reelin ligand controls the migratory behaviour of neurons by signalling through two major receptors: apolipoprotein E receptor 2 (ApoER2) and very low density lipoprotein receptor (VLDLR). Ectopic expression of reelin causes neuronal aggregations, formed of a cell-sparse central region analogous to the marginal zone (MZ) and a cell body-rich peripheral region similar to the primitive cortical zone (PCZ), in the developing neocortex. Although ApoER2 is required for this neuronal aggregate formation, the role of VLDLR remained unclear. Now, Yuki Hirota and Kazunori Nakajima show that, unlike ApoER2, VLDLR is not essential for neuronal aggregation but is required for the formation of the MZ-like structure, suggesting that VLDLR functions in MZ formation. Indeed, using GFP-labelled cortical neurons in Vldlr-KO mice, the authors show that Vldlr-deficient cells invade the MZ. By performing overexpression rescue experiments, they demonstrate that VLDLR suppresses neuronal invasion of the MZ in a cell-autonomous manner, potentially through regulating the activity of Rap1, integrins and Akt. Finally, the researchers demonstrate that Vldlr deficiency affects apical dendrite formation in pyramidal neurons. Together, these results reveal that the role of VLDLR is to prevent neuronal invasion into the MZ.