AbstractThe genetic factors known to be involved in the final realization of β‐glucuronidase activity in mice are considered from the standpoint ofstructural genesdetermining the catalytic activity of enzyme molecules as well as the recognition features of enzyme molecules that identify them for subsequent processing by the cell;processing genesdetermining the cellular apparatus involved with the conjugation, intracellular localization and eventual degradation of enzyme molecules;regulatory genesdetermining rates of enzyme synthesis, especially in response to physiological signals such as hormones; andtemporal genesdetermining the developmental programs for expression of these classes during growth and differentiation. The properties of genetic variants of β‐glucuronidase falling into each of these classes are described. When these results are considered in concert with the properties of genetic variants known for other mammalian enzymes several generalizations emerge. Structural genes of enzymes are not usually linked to the processing genes determining the postassembly events in the life of that enzyme. In contrast, all of the regulatory and temporal gene sites so far identified are in close proximity to the structural genes they modulate. Regulatory and temporal sites appear to act in acisfashion to control the amount of enzyme synthesized from the adjacent structural allele on the same chrom