In this work we provide evidence indicating that early expression of IGF-1R could be required for the normal orientation of cortical neuron precursors, with the Golgi complex oriented toward the cortical plate22. Migrating immature cortical plate neurons acquire a transient multipolar morphology in the VZ/SVZ. Then, after a polarity switch from multipolar to bipolar, they extend an axon at the upper IZ3, 4, 19, 20.This polarity switch is an important step during radial migration that has been implicated in specification of neuron subtype identity, cortical lamination, and projection formation3, 9, 23–25. Loss of function of the IGF-1R increases the proportion of neurons with multipolar morphology at the expense of bipolar cells in the RMZ. Therefore, IGF-1R is necessary for the polarity switch as well as neuronal migration, since most cells with knocked-down expression of IGF-1R remain arrested at the VZ/SVZ/IZ and are unable to form an axon, stopping neuronal polarity. We show that the IGF-1R acts through the activation of the PI3K pathway, as co- with shRNA-IGF-1R and a constitutively active form of PI3K rescues the migration defects.