It is important to note that alcohol-induced oxidative stress is dependent on the activity of the cytochrome P450 2E1 located in the endoplasmic reticulum; in the steatosis model used in this study, mitochondria play a significant role [2], and we were focused to know if HGF can also display a protective response in cells with mitochondria dysfunction as it does control NADPH oxidase- or Cyp2E1-mediated damage, in hepatic cells [5]. This evidence concerns the gene FMO5 and steatosis.