both dexamethasone-induced gene expression and depression and found in independent samples that this profile was predictive of depression as well as an overgeneralized amygdala response. Thus, it is possible to use GWAS derived summary statistics alongside additional targeted results to prioritize SNPs with both evidence of mechanistic function and disease association that may be more powerfully predictive than disease association alone. In this context, it would be important to show that such biologically-constrained PRS are not merely reflective of global genomic risk and indeed provide greater predictive utility.