These results should be interpreted in consideration of several limitations. First, we compared models of cross-disorder effects on the basis of the most often used goodness-of-fit measures, but other criteria might yield different results. For all four of the risk loci identified in the primary meta-analysis, the selected model had a substantially better fit than any alternative models had. However, for some loci that did not reach genome-wide significance, the difference in fit between our best-fitting and alternative models was moderate (appendix pp 38–45), so more than one model could be consistent with the noted effects. Second, diagnostic misclassification (eg, reciprocal misdiagnosis of cases of schizophrenia and bipolar disorder) could produce spurious evidence of genetic overlap between disorders.40 However, a substantial degree of misdiagnosis would be needed to account for our findings of loci that affect all or subsets of five disorders whose diagnostic criteria are fairly distinct. Third, the five disorders we examined were limited to those for which large-scale GWAS datasets have been assembled by the PGC and processed through a uniform quality-control process. As further datasets become
