By infinitesimal model, I mean the proposition that common variants are among the major source of genetic variance for disease susceptibility and continuous traits, where hundreds or thousands of loci contribute in each case. The loci detected by GWAS are merely the largest effect sizes drawn from a Poisson or similar distribution. If half a dozen common variants explain 10% of risk in the population, the remainder is attributable to a myriad of variants that each explain considerably less than 1% and have genotype relative risks less than 1.112. Figure 2a shows that affected individuals will tend to carry a slight excess of risk variants, since the overall distribution of the number of risk alleles per affected individual is skewed relative to unaffecteds. If these follow the same distribution of allele frequencies as neutral variation, then they will include a large number of rare variants as well. Ultimately, every gene contributes to every trait, but with effect sizes so small that it would take samples greater than the population size of the species to detect them. In practice, as shown
