reported a 240 kb duplication encompassing the EFCAB2 and KIF26B genes, and we found a 575 kb duplication of this region in one African-American patient. Thirdly, we also found two large duplications encompassing a reported 640 kb non-genic duplicated region on 4q35.2: 1.26 Mb in Munich and 1.28 Mb in Aberdeen. In summary, of 13 reported schizophrenia associated CNVs, we were able to find supporting evidence for 4 in our cohorts, including both of their highest-confidence regions [40]. Another study reported deletions of CNTNAP2 in schizophrenic patients [45], but we did not find any large events in this gene, and smaller deletions were present in both cases and controls. We next searched our cohorts for any of the 21 novel autosomic schizophrenia events reported by Walsh et al. [21]. We have already reported 2 Aberdeen and 1 US subject with the 1.4 Mb deletion on chromosome 1, which is now a known recurrent schizophrenia risk factor [22],[24]. Of the remaining 20, we found only 1 event that reoccurred in our samples: 2 Aberdeen cases had a 664 kb duplication at chr2:48625109–49290093. In a fourth study, Stone et al. (also using the Aberdeen cohort, genotyped with a different platform) reported the
