The population used by Walsh et al. contained a large number of young-onset and childhood-onset schizophrenia patients [21], a population one might expect to be enriched for genetic rather than environmental contributors. Like the Walsh et al., cohort, the Aberdeen schizophrenia cohort seems to contain an unusually large number of copy number variants both in comparison to the Aberdeen controls and in comparison to the other schizophrenia cohorts. However, the Aberdeen cohort was not enriched for young-onset patients, nor was it in any other obvious way different from the Munich patient cohort. The patients from both regions were selected using a consistent clinical protocol and the distribution of schizophrenia subtypes were similar. Further examination of population differences with those that do and do not carry an excess burden of large rare CNVs will be necessary to elucidate the differences between cohorts in this respect. Additionally, these differences seen in this study may in part depend on the type of platform used to detect the CNVs. The Aberdeen, Munich, and US cohorts were each genotyped using a different genotyping platform (Illumina
