Deficits in executive functions, especially cognitive function, are key features of SCZ. The roots of these deficits lie in cortical function and integration, at least in part tracing to the DLPFC. Here we have used gene expression derived from this tissue to understand how genetic liability is related to the molecular etiology of SCZ. Our analyses had two fundamental goals: to identify mechanisms that underlie genetic risk and to describe differences in gene expression and co-expression related to disease. By intersecting transcriptomics and genetics, we elucidated important aspects of the genetic control of transcription and found that genetic variants in 20 of the 108 SCZ GWAS risk loci alter expression of one or more genes. Prior analyses using brain eQTL datasets derived from older technologies have pointed to less than a handful of such associations3. In five of the 20 loci for which we observed regulatory potential of GWAS variants the risk variants altered expression of only one gene. Experimental manipulation of three of these genes had an impact on neuroanatomical and developmental attributes in model systems, making these genes
