Purpose of review <p>Alcohol consumption is a major contributor to the global cancer burden. This review synthesizes recent evidence on the epidemiology of alcohol use, the biological mechanisms underlying alcohol-related carcinogenesis, and the extent to which cancer risk is reduced following alcohol cessation. It also examines clinical and population-level strategies to reduce alcohol consumption.</p> Recent findings <p>Alcohol contributes substantially to cancer incidence, even at low levels of consumption. Acetaldehyde-mediated DNA damage, oxidative stress, and microbiome disruption are central carcinogenic pathways. Sustained alcohol cessation is associated with meaningful risk reduction for cancers of the oral cavity and oesophagus, whereas evidence for other cancer sites remains limited. Taxation, marketing restrictions, reduced availability, and brief interventions are the most effective approaches to lowering population-level alcohol exposure.</p> Summary <p>Coordinated action is required to reduce alcohol-attributable cancer burden. This entails implementing strong public health policies, improving surveillance, and promoting greater public awareness.</p>