Using ~270,000 SNPs, we created a genetic similarity matrix of over 8,000 unrelated individuals. By determining to what extent individuals' genetic similarity corresponded to their similarity in personality traits, we estimated the proportion of total personality trait variance that could be explained by the additive genetic effects of common causal variants that are associated with these SNPs. The variation explained by SNPs (4.2–9.9%) was statistically significant in three of the four traits, but for all four traits it represented a small proportion (~20%) of the total genetic variation previously estimated by various designs (twin, family, and adoption studies). The heritability estimated using the 270,000 SNPs captured the effects of the vast majority of common (MAF>0.01) causal variants, due to linkage disequilibrium between the SNPs and other common variants, but only a small portion of the genetic variation due to rare causal variants. As such, these results suggest that common additive genetic variants account for little of the variation in Cloninger's personality traits, and therefore rare genetic variants and/or some combination of dominance and epistasis are likely to account for most
