Alcohol consumption is associated with an inaeased risk of breast cance increasing linearly even with a moderate consumption and irrespectively of the type o alcoholic beverage. It shows no dependency from other risk factors like menopausal status, oral contraceptives hormone replacement therapy, or genetic history o breast cancer. The precise mechanism for the effect of drinking alcohol in mammary cancer promotion is still far from being established. Studies by our labora tory suggest that acetaldehyde produced in situ and accumulated in mamrnary tissue because of poor de toxicating mechanisms might play a role in mutational and promotional events. Additional studies indicated the production of reactive oxygen spedes accompanied of decreases in vitamin E and GSH contents and o glutathione transferase activity. The resulting oxida- tive stress might also play a relevant role in several stages of the carcinogenic process. There are reported in literature studies showing that plasmatic levels ofestrogens significantly increased after alcohol drinking and that the breast cancer risk is higher in receptor ER positive individuals. Estragens are known that they may produce breast cancer by actions on ER and also as chemical carcinogens, as a consequence of their oxida- tion leading to reactive metabolites. In this review we introduce our working hypothesis integrating the ac- etaldehyde and the oxidative stress effects with those involving increased estrogen levels. We also analyze potential preventive actions that might be accessible. There remains the fact that alcohol drinking is just one of the avoidable causes of breast cancer and that, at present, the suggested acceptable dose for prevention of this risk is of one drink per day.