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Full list of author information is available at the end of the articleBackground Non-alcoholic fatty liver disease (NAFLD), which is con-sidered a hepatic manifestation of the metabolic syn-drome, is currently one of the most common chronic liver diseases worldwide. NAFLD is classified into simple steatosis and non-alcoholic steatohepatitis (NASH), the latter being a severe condition of inflamed fatty liver that can, in time, lead to hepatic fibrosis, cirrhosis, he-patocellular carcinoma (HCC) development, and result in increased mortality (Chiang et al., 2011; Cusi, 2012; Siegel and Zhu, 2009). Steatohepatitis has been indi-cated by epidemiological studies to be a significant risk factor for developing HCC, at an annual HCC incidence of 2%–3 % in patients with NASH (Adams et al., 2005; Ascha et al., 2010). In 1998, Day and James proposed a “two-hit theory ” to explain NAFLD/NASH pathogenesis: the first hit, hepatic steatosis, increases the sensitivity of the liver to proinflammatory insults, while the second hi