The inheritance of two acetylator traits in a new mouse model of the human isoniazid acetylator polymorphism has been characterized. A/J mice have little or no blood p-aminobenzoic acid N-acetyltransferase activity and can excrete a low ratio of acetylsulfamethazine to sulfamethazine in urine. C57BL/6J mice have considerable blood p-aminobenzoic acid N-acetyltransferase activity and can excrete a high ratio of acetylsulfamethazine to sulfamethazine in urine. The expression of the blood p-aminobenzoic acid acetylation trait in F1, F2 and backcross progeny from A/J and C57BL/6J matings is consistent with simple Mendelian inheritance of two codominant alleles. Inheritance of in vivo acetylation rate, as measured by urinary ratio of acetylsulfamethazine to sulfamethazine, is independent of the blood acetylator polymorphism and is probably governed by simple Mendelian inheritance with incomplete dominance of low urinary ratio over high. Incomplete dominance appears to be limited to animals bearing one or two genes for rapid acetylation of p-aminobenzoic acid by blood hemolysates.