McLellan et al. (1997) characterized the distribution of CYP2D6 alleles among Saudi Arabians using restriction fragment length polymorphism (RFLP) analysis and allele-specific PCR amplification. A total of 101 individuals were genotyped, 21 of those had CYP2D6 gene duplication, whilst only two were heterozygous for a deletion of the whole gene. The frequency of the most common loss-of-function allele among Caucasians, CYP2D6*4, was only 3.5% in the Saudi population. Also, other alleles associated with decreased enzymatic activity, such as CYP2D6*10 and *17, were found at lower rates (3% each). Therefore, the prevalence of the poor metabolizer phenotype is relatively low among Saudi Arabians. Few years later, Lundqvist et al. (1999) presented evidence that CYP2D6 gene duplications occurred through unequal crossover at a breakpoint in the 3-prime flanking region of the CYP2D6*2B allele with a specific repetitive sequence. Alleles with 13 copies of the gene were likely formed by unequal segregation and extrachromosomal replication of acentric DNA. Lundqvist et al. (1999) suggested that the high frequencies of multiduplicated genes in Saudi Arabian and Ethiopian populations indicated that a dietary selective pressure existed in those regions in the past. These variants may have been introduced into the Spanish population during the Muslim migration.