Thus, for the first time, we now have a clear path to increased knowledge about the etiology of schizophrenia via application of standard, off-the-shelf genomic technologies for elucidating the effects of common variation. We suggest that a relatively thorough enumeration of the genomic loci conferring risk for schizophrenia (the “parts list”) should be a priority for the field. 8 Identifying all loci would surely be an exercise in diminishing returns. However, we propose a goal for the field: identification of the top 2,000 loci (for example) might be sufficient confidently and clearly to reveal the biological processes that mediate risk and protection for schizophrenia. Achievement of this goal would provide a strong empirical impetus for targeted biological and genetic research into the precise molecular basis of risk for schizophrenia, stratification of at-risk populations (e.g., psychotic prodrome), and appropriate cellular measure for evaluation of novel therapeutics. As indicated by our findings, greater knowledge of the genetic basis of schizophrenia can converge on increasingly specific neurobiological hypotheses that can be prioritized for subsequent investigation.
