Spatiotemporal regulation of neuronal migration is critical for the establishment of functional neural circuits. Disruption of neuronal migration during the development results in neuronal ectopia, which is associated with spontaneous seizures and increases the risk of epilepsy. In this talk, I will introduce our recent data regarding the impact of abnormal neuronal migration in epileptogenesis. We revealed that early-life febrile seizures induce the abnormal migration of dentate granule cells and future development of epilepsy. The abnormal migration was mediated by GABAergic excitation and resulted in the emergence of ectopic granule cells. Inhibition of the Na⁺K⁺2Cl^- co-transporter (NKCC1), which regulates the excitatory action of GABA, with a widely used diuretic bumetanide after the induction of febrile seizures rescued the abnormal migration and prevented the development of epilepsy. In addition, we found that febrile seizures enhance the dentate gyrus-mediated memory in adulthood, which was not observed in the presence of ectopic granule cells. The abolishment of ectopic granule cells with bumetanide rescued the attenuation of memory enhancements. Thus, we provide the experimental evidence that the prevention of neuronal ectopia exerts an anti-epileptogenic effect and modulates future memory after complex febrile seizures.