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Alcoholic liver disease (ALD) is a similar term denoting liver disorders encompassing steatosis, cirrhosis, and hepatocellular carcinoma. Recent evidence has suggested a vital role for epigenetic factors, which modulate gene expression in the absence of changes in DNA sequence, in the onset and progression of liver disorders, to foster hepatic fibrogenesis and cirrhosis. Mounting findings have delineated that alcohol consumption extensively modulates liver epigenetics, thus, prompting the etiology of ARLD and ALD. Alcohol\u2010induced epigenetic modifications (AIEM) in the liver encompass histone modification, microRNA\u2010induced genetic modulation, DNA methylation, and alcohol\u2010evoked cell signaling that alters gene expression. Herein, we aim at summarizing key findings to decipher AIEM and its role in the onset and development of ARLD and ALD from the perspectives of both cellular and animal models of alcohol exposure. 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