to ethanol-induced acute intoxication and alcohol preference in mice 13-15. Several neuroimaging studies have demonstrated that the uptake of acetate is significantly increased in the cerebellum and other brain areas after ethanol consumption in people with alcohol use disorder 14,16. The cerebellum is a primary brain region involved in alcohol metabolism and alcohol motor impairment. However, recent studies provide strong evidence for cerebellar contributions to non-motor functions such as cognition, language, emotions and social behaviours 17-19. The cerebellum also plays a role in many clinical neurological conditions, including attention deficit hyperactivity disorder, schizophrenia, bipolar disorder, major depressive disorder and anxiety disorders 20-22. Relative to the most frequently investigated brain regions, for example, the amygdala and basal ganglia, the cerebellum has been largely overlooked regarding its impact on neurological mechanisms underlying alcohol use disorder. Nevertheless, it remains unclear whether there is a central target that mediates ethanol-derived acetate production and acetate-induced behaviours. Specifically, we have only limited knowledge about the possible role of brain ALDH2 in alcohol metabolism and alcohol intoxication. One major barrier to our understanding of brain ALDH2 is a lack of specific approaches to distinguish between central and peripheral ALDH2-mediated

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