Breast cancer is a multifactorial disease that is triggered by gene–environment interactions. Epidemiological research has identified alcohol consumption as a significant non-hormonal-related and consistent risk factor, and is thus a preventable cause of breast cancer. The reasons why alcohol drinking increase breast cancer risk are unclear, and several hypotheses exist. The perturbation of estrogen metabolism and response appears to one mechanism underlying the association. Alcohol consumption also increases breast density in postmenopausal women and affects sex steroid levels. Other plausible mechanisms include: (1) mutagenesis by acetaldehyde, which is a metabolite of ethanol; (2) by enhancing the susceptibility of the mammary gland to carcinogenesis by affecting DNA repair, stimulating cell proliferation or altering mammary gland structural development; (3) influencing the disposition and function of essential nutrients or dietary factors considered cancer protective (e.g. affecting folate and one-carbon metabolism pathways); (4) inducing genome instability and DNA damage; and (5) inducing oxidative damage via ethanol or estrogen metabolism. To better understand the etiological nature of the effect of alcohol on breast carcinogenesis, further studies at the cellular and molecular levels on the interaction between ethanol and other risk factors, estrogen, carcinogens are needed.