Two women had each borne a child who had alpha1-antitrypsin (α1AT) deficiency Pi ZZ and who developed liver cirrhosis. In subsequent pregnancies, the women requested prenatal diagnosis. Samples of blood from the two fetuses were obtained at fetescopy. In a control group of five Pi MM fetuses aborted by hysterotomy, the mean α1AT level was 0.73 g/liter. Of the two fetuses at risk, one had an α1AT concentration calculated as 0.60 g/liter,i.e., within the Pi MZ range. The electrofocusing pattern indicated a heterozygous Pi MZ phenotype which was confirmed at birth. The other fetus at risk had a markedly decreased concentration of α1AT, 0.06 g/liter. Electrofocusing showed a homozygous Pi ZZ phenotype. Analysis of blood from the abortus confirmed these findings and thus the diagnosis of α1AT deficiency.