Using comparative genomic hybridization, Kirov et al. reported 13 possible schizophrenia associated CNVs [40]. One of these, a 1.4 Mb duplication including APBA2 and other genes was also found in our cohort and has already been discussed. The other CNV they designated as most likely to be pathogenic was a 250 kb deletion of 2p16.3 that included the 5′ end of NRXN1, a gene also implicated in two other recent studies [43],[44]. In our cohort we had three large deletions that encompassed the 3′ end of NRXN1 (200 kb in US, 260 kb and 420 kb in Munich), providing further evidence for this region in schizophrenia pathology. (It should be noted, however, that we also observed NRXN1 deletions in the cognitive normal extra control cohort, so all deletions in this gene should not be assumed to be pathogenic.) They also 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
