Our understanding of the fundamental genetic architectures of complex medical diseases and psychiatric disorders has expanded rapidly.73 It has also become manifestly clear that genomic searches for common variation via GWAS can successfully uncover biological pathways of etiological relevance. The major limitation to discovery is sample size.74 A recent GWAS for schizophrenia reported the identification of 22 genome-wide significant loci for schizophrenia (21,000 cases and 38,000 controls), and the results yielded multiple themes of clear biological and translational significance (e.g., calcium biology and miR-137 regulation).75 Moreover, given that cases and controls were derived from multiple sources and genotyped on multiple platforms, imputation was essential. Although effective, the preferred approach will always be to have samples genotyped on the same platform to maximize comparability and the capacity to identify genomic associations.
