Schizophrenia is a highly heritable disorder. Genetic risk is conferred by a large number of alleles and recently linkage analysis, candidate gene associations, and genome-wide association analyses (GWAS) have provided some advances to the field. However, a major limitation in the field is the fact that expression and other studies have been limited to analysis of blood samples or postmortem brain tissue while the functional studies for the identified mutation or CNV are conducted in animal models or cell lines. To address this gap, we have collected skin biopsies and generated fibroblast lines for large number of patients including some with known, recurrent CNVs that have been implicated in schizophrenia risk as well as for similar number of matched controls. We are using a similar approach as for the autism spectrum disorder project and are reprogramming iPSCs from these fibroblasts to generate NPCs and then mature neurons. We will examine both genome-wide expression changes and cellular phenotypes in neural cells derived from patients with schizophrenia compared to cells derived from healthy control and expect to discover biological pathways disrupted in schizophrenia.