Significance Increased mammalian target of rapamycin complex 1 (mTORC1) signaling is associated with many neurological and neurodevelopmental disorders, ranging from epilepsy to autism, that feature developmental defects in the organization of the cortex. Despite the fact that much research has focused on mTORC1-related disorders, the downstream effectors that produce these developmental defects are not well understood. To begin filling that void, this study looked at the role of one of the many cellular processes regulated by mTORC1, cap-dependent translation. Surprisingly, normalizing signaling through only one of mTORC1’s targets [eukaryotic initiation factor 4E-binding proteins (4E-BPs)] was able to block ectopic placement of cortical neurons, and mimicking mTORC1 signaling through 4E-BP alone was sufficient to induce neuron misplacement.