Genome-wide association studies in human populations have facilitated the creation of genomic profiles which combine the effects of many associated genetic variants to predict risk of disease. Genetic testing has long been available for Mendelian genetic diseases for which variants within one gene are directly responsible for the disease. In contrast, the etiology of complex genetic diseases, such those listed in Table 1, comprises both genetic and environmental risk factors. Results from genome-wide association studies have provided empirical evidence that very few associated genetic variants with effect size greater than odds ratio of 1.5 exist [1],[2]. Reconciliation of these effect sizes with the, often sizeable, estimates of heritability for many complex diseases (Table 1) means that we must expect there to be many (perhaps thousands) of genetic variants underlying complex disease if the effect size of any one variant is very small. It follows that each individual will carry a different, probably unique, portfolio of risk alleles. Whereas common risk variants have size too small to be used individually as risk predictors, profiles based on many associated genetic variants could
