might be increased in large multicenter samples; e.g., despite the generally high inter-rater reliability for these disorders, research groups can have diagnostic “biases”, some of which could correlate with specific risk alleles. But power increases with sample size despite some degree of misclassification, which also occurs in many medical disorders for which there are GWAS findings.More needs to be learned about the selection of controls for psychiatric GWAS studies. It remains possible that some findings will be confounded by systematic biases in control groups, such as under-representation of developmental disabilities. In any event, the field will need much larger control groups ascertained by diverse methods and from multiple ethnic populations.For some disorders, there might be no detectable main effects of SNPs, only higher order gene-gene or gene-environment interactions. However, main effects are often detectable even if interactions are erroneously excluded. Explicit tests of interactions (74) or data mining might prove informative.GWAS assays do not interrogate all common variants. For each array type, some assays perform poorly, and some common SNPs are not or cannot be tagged.Improved methods will be needed to provide more systematic information about CNVs and their relationship to disease. Associated CNV regions will require resequencing studies of