that are not well tagged by the SNPs included in the genotyping platforms. The UGT complex of genes, which catalyze nicotine and cotinine glucuronidation [34], were significant in both the OZALC-NAG and SAGE studies, and were identified among the other retinoid binding genes. Furthermore, the flavin monooxygenase 1 gene (FMO1) is also associated with nicotine metabolism [42] and was tagged in the three studies. There is one KEGG pathway (hsa00982 “Drug metabolism – cytochrome P450”) and two GO terms (GO:0005792 “microsome” and GO:0042598 “vesicular fraction”) with less than 500 genes that include FMO1 and UGT1A4. However, each of these terms and pathways has a very large number of genes (i.e., 73, 241 and 248 genes respectively); and thus are not specific enough to formally represent nicotine metabolism genes. In contrast, the identification of ribosome genes was an unexpected result of our analysis. The relationship, if any, of this gene family to nicotine consumption is not currently understood.
