It has been hypothesized that progression through NAFLD stages involves multiple adverse “hits” where both hepatic inflammation and oxidative stress are key facilitators . Accordingly, serum and hepatic levels of proinflammatory cytokines such as tumor-necrosis factor alpha (TNF-α) and monocyte-chemoattractant protein-1 (MCP-1) have been found to be increased in patients with both simple hepatic steatosis and NASH [6–9]. Also, the glycoproteins haptoglobin and tissue-inhibitor of metalloproteinase 1 (TIMP-1) have been shown to be elevated in plasma of patients with more advanced stages of NAFLD and have therefore recently been suggested as useful clinical plasma biomarkers, indicative of hepatocyte ballooning and liver fibrosis, respectively [10, 11].