Accordingly, alcohol intake could decrease AMPK expression, which activated lipogenic enzymes through upregulating the level of sterol regulatory element-binding protein (SREBP) and downregulating the level of peroxisome proliferator- activated receptor α (PPARα), thereby inducing lipid accumulation, suppressing mitochondrial fatty acid oxidation or export, and ultimately leading to hepatic steatosis [5,25,26]. The gene discussed is CNBP; the disease is fatty liver disease.