Comparison of subjects grouped by CYP2A6 diplotype using both metabolism metrics, log(D2-cotinine: D2-nicotine) and D2-cotinine: (D2-nicotine + D2-cotinine)), (Table 4) yields three primary novel findings: 1) the similarity between the CYP2A6*12 allele and the known null alleles *2 and *4; 2) the significant difference between the *1A(51A) allele and other presumed fully-functional alleles, including *1B; and 3) the similarity between the *1B allele and other alleles, notably *1D. The third finding suggests that the previously reported [27]influence of the *1B 3′ UTR conversion (Table 1) on nicotine metabolism is due overwhelmingly to the difference between *1B and *1A(51A), not the presence of the 3′ UTR conversion itself. The three slowest nicotine metabolizers measured among these 189 subjects were genotyped as *4/*12, *4/*2 and *12/*1D-Y351H (D2-cotinine: (D2-nicotine + D2-cotinine) = 28%, 34% and 44% respectively, compare to Table 3) leading to the hypothesis that the CYP2A6*12 allele might be equivalent to the two null alleles, *4 and *2 in respect to nicotine metabolism. ANOVA analysis provided no evidence of a difference between heterozygotes (excluding the three above-mentioned subjects) for the CYP2A6*12,
