In the past few years, despite the phenomenal increase in the number of published GWAS and in the number of replicated associations for complex human diseases [Hirschhorn 2009; Manolio, et al. 2008], much of the genetic variation in disease traits remains unexplained by SNP associations detected so far. One possible explanation is that the variance is due to a large number of SNPs with small effects, in which case many more loci might be detected as power increases with increasing sample size. Studies with very large sample sizes, on the order of tens of thousands of subjects, have more power, but are also more likely to be affected by experimental errors. Therefore, QC/QA of genotypic data in GWAS will continue to be an important aspect of human genetics research.
