In view of the apparent conflict between the observations of high proportions of additive genetic variance (often half or more of the phenotypic variance, and even more of the total genetic variance) and the recent reports of epistasis at quantitative trait loci (QTL) [8], we consider explanations beyond that of simple sampling errors and bias of estimates. We focus particularly on the role that the distribution of gene frequencies may play in the relation between the genetic model and the observed genetic variance components.
