Cortical malformations, including Focal Cortical Dysplasia type II (FCDII), are common causes of pediatric epilepsy. FCDII is characterized by abnormal cortical lamination and cytomegalic cells. Recently, deep sequencing of surgically resected brain tissue has revealed somatic mutations in mTOR pathway genes in up to 60% of FCDII-cases. Since available human FCDII samples reflect an advanced disease stage, the developmental origins and mechanisms, including the cell types affected by pathogenic mutations and their impact on cell-type-specific transcriptional programs, remain unknown. We aim to generate an inducible mosaic MTOR organoid model that mimics the disease etiology. First, we selected the MTOR S2215F variant, as it is one of the most frequent mutations found in FCDII. Second, the MTOR S2215F variant will be expressed only in a small subset of cells to model the low-degree mosaicism as in FCDII patients. Third, we will make the expression of MTOR S2215F inducible using a FLEX-Cre switch system, enabling us to express the variant at different time points. We will assess the differential effect on the FCDII phenotype by monitoring the mTOR pathway activity and the presence of cytomegalic and heterotopic cells. The introduction of the mutation at different time points will shed light on the specific timeframe during which mutations occur in FCD patients and enable us to select the optimal timing for replicating an FCDII-like phenotype in our model. The next step will include single-cell transcriptomic profiling to uncover the cellular and molecular mechanisms behind FCDII development.