Current approaches to population genetics focus on evolutionary information extracted from genomics, where large-scale sequencing is telling us much about the operation of natural selection. Within this field an important issue is the nature and evolution of genetic dominance. Historically, inheritance in natural populations was viewed in terms of dominant ‘‘wild-type’’ alleles, following the discovery of the reserve of recessive alleles present as heterozygotes in wild Drosophila as revealed by inbreeding (reviewed by Keightley 1994). This reserve was thought to provide the feedstock for evolution in response to environmental change, a view that the new genomics has verified and much extended, not only in man but also in natural animal and plant populations (Eyre-Walker and Keightley 2007; Mitchell-Olds et al. 2007). The importance of inheritance pattern is not confined to the human population. The relative contribution of dominant and recessive variation is an important consideration in animal and plant breeding and in the management of wild populations (Edmands 2007). Inbreeding depression, the hallmark of recessive inheritance (and sometimes of heterozygous advantage), has long been known as an important factor in the design of agricultural breeding programs (Falconer 1989). Experimental mutagenesis potentially can provide information valuable for population genetics. A key procedure in the new genomics is to compare a variable that is subject to natural selection with a control variable supposedly unaffected in this way, typically nonsynonymous compared with synonymous nucleotide substitution (although there is evidence of at least some selection on synonymous mutations). This type of analysis has not yet been applied to the population genetics of dominance because of the lack of an appropriate neutral control. Our purpose here is to inquire how data from mutagenesis might fill this gap. The form of information from mutagenesis most relevant to man is the relative frequencies of mutants in the first (G1) and third (G3) generations in mice. Provided selective effects within the mutagenesis screen can be avoided, this ratio should provide an estimate of the dominant and recessive relative mutation rate that is unaffected by natural selection. The ratio could then be compared with the ratio recorded for human monofactorial disease, where natural selection has operated over many generations on recessive but not on dominant mutant alleles. Our purpose here is to alert the mutagenesis community to this need for G1:G3 ratio data. In addition, the dominant and recessive mutants, as they accumulate, should contribute much to understanding the cell biology of dominance.