The debrisoquine-4-hydroxylase polymorphism is a genetic variation in oxidative drug metabolism characterized by two phenotypes, the extensive metabolizer (EM) and poor metabolizer (PM). The 4‘-hydroxylation of debrisoquine is mediated by CYP2D6, and the polymorphism, inherited as an autosomal recessive trait, is a clinically important defect affecting 5–10% of individuals in Caucasian populations (Brosen & Gram, 1989). The absence of CYP2D6 activity in PM livers is caused by one of several molecular defects (Heim & Meyer, 1990). A point mutation at the 3’-splice site of intron 3(CYP2D6(B)mutation), a single nucleotide (A) deletion in exon 5(CYP2D6(A)mutation) and aCYP2D6gene deletion all lead to defective mRNA and/or protein and thus, a deficiency in CYP2D6 activity.Polymerase chain reaction (PCR) based methods have recently been developed to detect these mutations, resulting in approximately 95% of individuals being correctly phenotyped (Goughet al, 1990; Heim & Meyer, 1990).This paper reports the development of a simple PCR analysis that detects the two major mutations,CYP2D6(A)and(B), in a single analysis, and also confirms previous analyses (Evans & Relling, 1991) reporting the presence of less frequently occurring mutations. Also illustrated is the importance of extra analyses, or the due caution that is required, when predicting phenotype from genotype in individuals that are heterozygous at both the A and B loci.