We have summarised empirical evidence for the existence of non-additive genetic variation across a range of species, including that presented here from twin data in humans, and shown that most genetic variance appears to be additive genetic. There are two primary explanations, first that there is indeed little real dominant or epistatic gene action, or second that it is mainly because allele frequencies are distributed towards extreme values, as for example in the neutral mutation model. Complete or partial dominance of genes is common, at least for those of large effect; and epistatic gene action has been reported in some QTL experiments [8],[69]. Detailed analyses in Drosophila melanogaster, using molecular and genetic tools available for it, identify substantial amounts of epistasis, including behavioural traits [70] and abdominal bristle number [71], yet most genetic variation in segregating populations for bristle number appears to be additive (as noted above). But many QTL studies of epistatic gene action suffer from a high degree of multiple testing, increasingly so the more loci and orders of interaction are included, such that they may be exaggerating
