Alcoholic fatty liver disease (AFLD) is considered as one most prevalent disease in today’s world. A common reason for this condition is the long-term consumption of alcohol. Various studies known are supposed to make a guess that the prevalence rate of fatty liver disease will increase by 2–3 times by the year 2030. Recent data documented from the National Health and Nutrition Examination Survey (NHANES) report that the occurrence rate of AFLD associated with the consumption of alcohol in adults is around 4%. All compounds are meant to be stable via the pairing of electrons; meanwhile the involvement of unpaired electron causes the generation of an extremely reactive or unstable molecule. Such molecules are considered as free radicals. The free radicals formed by oxygen are called reactive oxygen species (ROS). The liver is considered as the main organ associated with the metabolism of alcohol and also the main affected organ by alcohol-induced diseases. The succession of AFLD consists of a series of steps such as steatosis, steatohepatitis, and then cirrhosis. A study has shown that a ten times thick fold of triglycerides in the liver was observed in mice after the consumption of high dose of alcohol. The ordinary pathway concerned with the processing of alcohol is via acetaldehyde through the enzyme alcohol dehydrogenase in the cytosol. The end results are liver cell death, activation of the hepatic stellate cells that lead to scarring, and disrupted lipid metabolism. This exacerbates the accumulation of fat in the liver. Future treatment methods need to target the interruption of this cycle.