A growing body of evidence suggests three generalities about the a-chain hemoglobin genes in mammals: 1) the loci are almost always present in duplicate copies; 2) the duplicate loci are closely linked on the chromosome; and 3) the duplicate loci produce subunits in unequal amounts, usually in a ratio roughly approximating 2:1. The first purpose of this report is to confirm and extend those conclusions vis-avis the deer mouse, Peromyscus maniculatus. Deer mice show a very diverse range of hemoglobin phenotypes, due to polymorphisms at multiple hemoglobin loci (Rasmussen et al., 1968; Jensen et al., 1976; Maybank and Dawson, 1976; Snyder, 1977, 1978a, 1978b). Previous genetic data and molecular structure studies have demonstrated that at least two of the five hemoglobin structural loci code for a-type globins (Snyder, 1978a). Through the use of comparative linkage data it has been possible to identify the a-globin loci as those previously designated as Hba and Hbc (Snyder, 1980). As reported here, the discovery of a second electrophoretic allele at the Hba locus has made it possible to map the a-globin loci. Also, the use of thin-layer isoelectric focusing has revealed additional Hba and Hbc alleles and has made it possible to determine the genotypes of a number of previously ambiguous phenotypes. That, in turn, has allowed precise measurements of the relative amounts of subunits produced by the two a-globin loci. The second purpose of this paper is to reconcile conflicting views about the evolutionary history of the duplicate a-globin loci. The unequivocal occurrence of duplicate a-globin loci in diverse orders of mammals-and their probable occurrence in all mammals-implies that a single duplication of an ancestral a-globin locus took place before the evolutionary radiation of the mammals. On the other hand, amino acid sequence data indicate that, typically, there are more differences between a globins from separate taxa than there are between the duplicate a globins within a taxon. That general result has been interpreted to mean that in most mammalian taxa the duplication of the aglobin loci occurred rather recently in evolutionary time. The point made here is that there are at least two simple and feasible genetic mechanisms whereby the products of an ancient gene duplication can continue to evolve in concert and thereby contribute to the adaptive radiation of mammals.