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There has been a recent flurry of papers about the effects of an individual's genetic make-up on their risk of addiction to smoking and of developing smoking-related illness. One important culprit is the gene CYP2A6 encoding the drug-metabolising enzyme cytochrome P-450 2A6. CYP2A6 catalyses an important step in the metabolism of nicotine. About 20% of the white population carries at least one copy of the gene that is non-functional (encoded by a 'null allele' of the gene), and around 1% have two non-functional copies. These percentages vary in different populations, for example they are much lower in African Americans, only 2.5% of whom carry a non-functional allele. A recent paper in the Scientific Correspondence section of Nature [Pianezza, M.L., Sellers, E.M. and Tyndale, R.F. (19980 Nature 393, 750] reports that 'poor metabolisers' (people with at least one null allele) are less likely to become addicted smokers and, if they do smoke, tend to smoke fewer cigarettes. CYP2A6 is also involved in formation of an activated carcinogen from one of the chemicals in tobacco smoke, so fast metabolisers may also be at increased risk of lung cancer, as is observed for African American smokers [see Editorial by Sellers, E.M. (1998) JAMA 280, 179-180].

Comment: No single gene can account for the 'pharmacogenetics' of smoking. Nevertheless, the time may not be far off when it will be possible to identify sets of gene variants that make individuals particularly susceptible to nicotine addiction and/or smoking-related illness. It seems clear that the most sensible public-health policy will always be to discourage anyone from smoking, but if further research confirms the differential susceptibility of different racial groups, for example, there may be a case for targeting part of the anti-smoking campaign preferentially at vulnerable subsets of the population.