Inherited quantitative aspects of the Rh blood-group system and susceptibility of Rh to the effects of independently segregating suppressor genes can be accounted for with a conjugated operon model. This assumes the existence of four operator or promotor (control) genes for these functions, while closely linked structural regions determine the qualitative characteristics of Rh antigens. Observed restriction of antigenic crossreactivity to the products of adjacent genetic regions and data from blood typing of nonhuman primates both suggest that Rh complexity arose from a series of gene duplications and independent mutations.The 33 qualitatively different antigenic specificities of the Rh blood-group system (1, 2) have become extraordinarily difficult to organize systematically. Each allele at the Rh locus determines a variable number of different antigens (3,4), and recombination has been observed in just one family (5). In addition, quantitative differences in the expression of Rh antigens are also under the control of Rh genes (6). Accommodation of quantitative data by genetic theories devised to account only for qualitative alloantigenic variants (3,4,7,8) results in a vast increase in an already overwhelmingly large number of complex alleles.In this report, Rh data have been arranged in a manner that distinguishes qualitative from quantitative information. From this arrangement, a consistent genetic model emerges that may provide a biologically sounder conceptual basis for this complex system.In the Rh system (see Table 1 for glossary of terms) Rh: wl (Rh or DU) was the first quantitative variant found (9). A most interesting situation was shown to involve allelic interaction, with the R-",2 -3 (r' or dCe) gene being suppressive of RI alleles (R or D) in trans position (10). Quantitative variants of RI were documented quantitatively by Silber et al. (11) and Masouredis (12), but Gibbs and Rosenfield (6) found that the quantitative "degree of expression" was under the strict genetic control of Rh genes and so was the interallelic depressive effect of R-1"2 -3. Within an extensive pedigree, identical genotypes were quantitatively identical for four different Rh antigens, whereas qualitatively similar genotypes in the general population varied over a significant range (6). Using a different method, Berkman et al. (13) confirmed these observations and extended the findings to the other blood groups.