It is now possible to represent the majority of common genetic variation by genotyping a selected set of tagging SNPs [16]. Such hypothesis-free genome-wide association studies allow the discovery of new genes and pathways affecting complex traits such as schizophrenia with much greater power to detect small effects than linkage studies. To date, there have been five genome-wide association studies (GWAS) of schizophrenia. The first study used a small sample size of 178 cases and 144 controls self-identifying as Caucasian and recruited in the US, and reported the association of a SNP in the pseudoautosomal region of the y chromosome at p = 3.7×10−7 [17]. The second used pooled DNA samples from 600 cases and 2,771 controls, all Ashkenazi Jews, and found no genome-wide significant association, although they reported a strong effect of a RELN SNP in females only [18]. The third used pooled DNA from 574 schizophrenia trios and 605 unaffected controls, all recruited in Bulgaria and again found no genome-wide significant association [19]. The next study of 738 cases and 733 controls (each about 30% African-American, 56% European
