The GATOR1 complex, particularly the NPRL2 gene, is thought to play a pivotal role in neuronal development and cellular organization within the cerebral cortex, yet it has been poorly characterized. Dysregulation of this gene has been implicated in focal cortical dysplasia type 2 (FCD2), a neurodevelopmental disorder characterized by mTOR pathway hyperactivation, cortical dyslamination, and epileptogenicity. This dissertation aims to characterize the role of Nprl2 in FCD2 pathogenesis, employing a combination of in vitro and in vivo approaches to elucidate the effects of Nprl2 knockout on cellular morphology and circuit function. Using CRISPR/Cas9 to knockout Nprl2 in N2a cells and primary cortical neurons from in utero electroporated Nprl2 KO mice, I demonstrated that Nprl2 KO leads to pronounced soma enlargement, enhanced dendritic arborization, and increased cellular aggregation—features consistent with hyperactive mTOR signaling. Notably, these phenotypic changes were mitigated by rapamycin, underscoring the therapeutic potential of mTOR inhibitors in FCD2. In vivo, focal Nprl2 KO via in utero electroporation induced cortical dyslamination, mTOR pathway hyperactivation, and soma enlargement, all of which were reversed by rapamycin treatment. However, the reduced seizure threshold observed in Nprl2 KO mice was not completely rescued by rapamycin, suggesting that Nprl2 may affect seizure susceptibility through additional mechanisms. Electrophysiological analysis using whole-cell patch clamp techniques further revealed increased capacitance and decreased action potentials in Nprl2 KO neurons, implicating Nprl2 in the modulation of neuronal excitability. Together, these findings highlight Nprl2 as a key regulator of cortical structure and function, offering insight into potential therapeutic targets for cortical malformations associated with epilepsy.