further suggests that this relationship might be clinically relevant. This was particularly well illustrated by the response of the transcriptome to cigarette smoking. We showed that less than 20 genes among the 12,000 expressed in monocytes could highly discriminate smokers and non-smokers, and among them, four genes were sufficient to account for the strong association existing between smoking and atherosclerosis. Whether these genes are causally involved in the mechanisms linking smoking to the development of atherosclerotic plaques or whether they are only markers of ongoing pathological processes remains to be elucidated.
