reflecting a selection of SNP sets based on biological processes (for example, signaling pathway membership, protein–protein interactions, or pharmacological treatment response) have been calculated and applied 11, 12. These pathway-specific PRS may predict phenotypic variation more robustly than risk scores reflecting overall disorder risk and may be more amenable to mapping of specific endophenotypes or phenotypic correlates of disease (such as cognitive and cortical changes which are associated with the disorder or its symptoms) 13– 15.
