Tirzepatide, a dual GLP-1 and GIP receptor agonist approved for diabetes and weight management, demonstrated potent anti-alcohol effects across multiple rodent models. The drug reduced alcohol's rewarding properties by blocking dopamine release in the nucleus accumbens, decreased voluntary alcohol consumption in a dose-dependent manner, and prevented both binge drinking and relapse behaviors even with repeated dosing. Mechanistically, tirzepatide induced sustained synaptic depression in the lateral septum while altering histone regulatory proteins in this brain region. This finding represents a potentially significant advance for alcohol use disorder treatment, which currently has limited pharmacological options. The dual receptor mechanism distinguishes tirzepatide from earlier GLP-1-only compounds that showed modest anti-addiction effects. However, translating these rodent findings to humans remains uncertain, particularly regarding optimal dosing and whether the anti-alcohol effects can be separated from appetite suppression and weight loss. The epigenetic changes in histone proteins suggest tirzepatide may create lasting neuroadaptations that could sustain recovery, though this requires validation in clinical populations where addiction involves complex psychological and social factors beyond neurochemical reward pathways.