Early genomic studies in psychiatry assumed that there might be one or a handful of major effect genes or loci (that is, that psychiatric conditions were monogenic or oligogenic) and that identification of these key risk genes would provide clear insights into disease mechanisms. After decades of studies which failed to find a consistent signal using these simple genetic models, the field moved toward the understanding that most common psychiatric disorders are both polygenic and genetically heterogeneous (that is, where many tens or hundreds of genetic loci influence disease risk and where the combination of risk alleles is different in different people). This was a paradigm shift in the thinking of researchers 4; with it came the realization that the sample sizes which were able to be collected by a single investigator or group were not going to provide sufficient power to clearly detect genetic effects, most of which would be quite small individually (though substantial in combination). New and more efficient molecular technologies reduced the costs of genome-wide genotyping, and large-scale highly collaborative approaches—such as those conducted by the
