Despite its relatively low hepatic abundance (≈5–7% of human hepatic P450 content), its ability to bioactivate xenobiotics into toxic/reactive intermediates and its high propensity for inciting oxidative stress have implicated CYP2E1 in the pathogenesis of toxic liver damage, alcoholic liver disease, nonalcoholic steatohepatitis (NASH), diabetes and obesity [5,6,7,8,9,10,11,12,13,14]. This evidence concerns the gene CYP2E1 and Obesity.