The CommonMind Consortium sequenced RNA from the dorsolateral prefrontal cortex of schizophrenia cases (N = 258) and control subjects (N = 279), creating a resource of gene expression and its genetic regulation. Using this resource, approximately 20% of schizophrenia loci have variants that could contribute to altered gene expression and liability. In five loci, only a single gene was involved: *FURIN*, *TSNARE1*, *CNTN4*, *CLCN3*, or *SNAP91*. Altering expression of *FURIN*, *TSNARE1*, or *CNTN4* changes neurodevelopment in zebrafish; knockdown of *FURIN* in human neural progenitor cells yields abnormal migration. Of 693 genes showing significant case/ control differential expression, their fold changes are ≤1.33, and an independent cohort yields similar results. Gene co-expression implicates a network relevant for schizophrenia. The findings show that schizophrenia is polygenic and highlight the utility of this resource for mechanistic interpretations of genetic liability for brain diseases.The CommonMind Consortium sequenced RNA from the dorsolateral prefrontal cortex of schizophrenia cases (N = 258) and control subjects (N = 279), creating a resource of gene expression and its genetic regulation. Using this resource, approximately 20% of schizophrenia loci have variants that could contribute to altered gene expression and liability. In five loci, only a single gene was involved: *FURIN*, *TSNARE1*, *CNTN4*, *CLCN3*, or *SNAP91*. Altering expression of *FURIN*, *TSNARE1*, or *CNTN4* changes neurodevelopment in zebrafish; knockdown of *FURIN* in human neural progenitor cells yields abnormal migration. Of 693 genes showing significant case/ control differential expression, their fold changes are ≤1.33, and an independent cohort yields similar results. Gene co-expression implicates a network relevant for schizophrenia. The findings show that schizophrenia is polygenic and highlight the utility of this resource for mechanistic interpretations of genetic liability for brain diseases.