which are recognized as a potential precursors of cirrhosis and hepatocellular carcinoma. Emerging evidence indicates that oxidative stress and dysregulation of redox-sensitive signaling pathways are central to the pathobiology of fatty liver diseases [1]. The role of liver steatosis, which affects around 30% of the general population, in development of liver deteriorations still remains unclear. Reactive oxygen species (ROS) are by-products of normal cellular metabolic processes. When ROS exceed certain level and not adequately removed, the balance between pro- and antioxidants is impaired, resulting in oxidative stress [2]. Oxidative stress can lead to the modifications of biological molecules, including DNA, lipids and proteins and has been implicated in many pathological conditions [3,4]. Recent data emphasize the importance of the local sites of ROS generation [2,3,5,6]. Some analysis have shown that the relative redox states from the most reducing to the most oxidizing can be assigned as mitochondria4nuclei4cytoplasm4 endoplasmic reticulum4extracellular space [2]. However, it is logical to speculate that at specific conditions, when ROS production has been augmented in one of the cellular compartments, this equation will no longer be accurate.