These new findings [5] raise some interesting mechanistic issues. Considering ADH1B first, the protective effect of the ADH1B 48H allele initially seems intuitive, in that a more rapid clearance of ethanol would be associated with reduced cancer risk. This idea, however, is difficult to reconcile with the other evidence from ALDH2-deficient individuals which suggests that it is acetaldehyde, rather than ethanol itself, that is responsible for oesophageal carcinogenesis associated with alcohol drinking. There are at least two possible explanations for this conundrum.
