The CommonMind Consortium (CMC) analyzed gene expression in the dorsolateral prefrontal cortex (DLPFC) of 258 schizophrenia (SCZ) cases and 279 controls, generating a resource of gene expression and its genetic regulation. Using this data, ~20% of SCZ loci showed variants that could affect gene expression and liability. Five loci involved only one gene: FURIN, TSNARE1, CNTN4, CLCN3, or SNAP91. Altering expression of these genes affected neurodevelopment in zebrafish and human neural progenitor cells. Of 693 genes with significant case/control differential expression, fold changes were ≤1.33, and an independent cohort showed similar results. Gene co-expression implicated a network relevant to SCZ. The findings show SCZ is polygenic and highlight the utility of this resource for understanding genetic liability for brain diseases. The CMC identified 2,154,331 significant cis-eQTLs for 13,137 genes. Many eQTLs for the same gene were highly correlated, and 32.8% of eSNPs predicted expression of more than one gene. Cis-eQTLs were enriched in genic elements and non-coding RNAs, particularly within 100 kb of the transcription start and end sites. An "eGene" is a gene with at least one significant eSNP. The CMC identified 8,427 eGenes at FDR ≤5%. Cis-eQTLs were enriched for enhancer sequences present in brain tissues. The CMC also identified 45,453 significant trans-eQTLs at FDR ≤5%, with 20,288 also being cis-eQTLs for local genes. The CMC identified 73 out of 108 SCZ GWAS loci with cis-eQTLs. Of these, 84 genes in 30 loci showed co-localization of GWAS risk and eQTL association signals. The CMC identified 33 genes in 18 of the 108 GWAS loci. These genes were enriched for nonsynonymous de novo mutations in autism. The CMC also identified nine genes in eight GWAS loci using isoQTLs. These genes showed evidence that mis-regulated gene expression could explain the genetic association with schizophrenia. The CMC identified five single-gene loci encoding known proteins implicated at the gene level. These genes were tested in the ROS/MAP study and showed significant eQTLs. CLCN3, SNAP91, and TSNARE1 are direct synaptic components, while CNTN4 and FURIN play roles in neurodevelopment. FURIN processes precursor proteins to mature forms, including BDNThe CommonMind Consortium (CMC) analyzed gene expression in the dorsolateral prefrontal cortex (DLPFC) of 258 schizophrenia (SCZ) cases and 279 controls, generating a resource of gene expression and its genetic regulation. Using this data, ~20% of SCZ loci showed variants that could affect gene expression and liability. Five loci involved only one gene: FURIN, TSNARE1, CNTN4, CLCN3, or SNAP91. Altering expression of these genes affected neurodevelopment in zebrafish and human neural progenitor cells. Of 693 genes with significant case/control differential expression, fold changes were ≤1.33, and an independent cohort showed similar results. Gene co-expression implicated a network relevant to SCZ. The findings show SCZ is polygenic and highlight the utility of this resource for understanding genetic liability for brain diseases. The CMC identified 2,154,331 significant cis-eQTLs for 13,137 genes. Many eQTLs for the same gene were highly correlated, and 32.8% of eSNPs predicted expression of more than one gene. Cis-eQTLs were enriched in genic elements and non-coding RNAs, particularly within 100 kb of the transcription start and end sites. An "eGene" is a gene with at least one significant eSNP. The CMC identified 8,427 eGenes at FDR ≤5%. Cis-eQTLs were enriched for enhancer sequences present in brain tissues. The CMC also identified 45,453 significant trans-eQTLs at FDR ≤5%, with 20,288 also being cis-eQTLs for local genes. The CMC identified 73 out of 108 SCZ GWAS loci with cis-eQTLs. Of these, 84 genes in 30 loci showed co-localization of GWAS risk and eQTL association signals. The CMC identified 33 genes in 18 of the 108 GWAS loci. These genes were enriched for nonsynonymous de novo mutations in autism. The CMC also identified nine genes in eight GWAS loci using isoQTLs. These genes showed evidence that mis-regulated gene expression could explain the genetic association with schizophrenia. The CMC identified five single-gene loci encoding known proteins implicated at the gene level. These genes were tested in the ROS/MAP study and showed significant eQTLs. CLCN3, SNAP91, and TSNARE1 are direct synaptic components, while CNTN4 and FURIN play roles in neurodevelopment. FURIN processes precursor proteins to mature forms, including BDN