The brain is a genetic mosaic, meaning that individual neurons harbor unique genotypes distinct from one another and distinct from the individual’s inherited genetic code. This phenomenon is attributed to mutations that arise in neural progenitors during prenatal development. The result is a mosaic brain where cells are defined by a signature of single nucleotide variants, copy number variation, and retrotransposon insertions. Each somatic variant has the potential to influence the function of its host cell and the wider neuronal network. To some extent, brain mosaicism likely contributes to normal neuronal diversity and complexity. But brain mosaicism has also been linked to disorders ranging from structural brain abnormalities to epilepsy and psychiatric disease. Our lab is interested in genetic mechanisms that shape the developing brain and contribute to neurodevelopmental disease. We use a translational approach that combines characterization of patient brain specimens with functional modeling in patient-derived cell lines and transgenic mice. We are addressing fundamental questions related to how genetic mosaicism affects neurodevelopment during health and disease, such as how somatic mutations arise and populate the brain, how they affect individual cells and the larger network/structure, how a small number of affected cells have a widespread effect, and how somatic mutations contribute to complex phenotypes.