 Obesity, diabetes, hypertriglyceridemia, hypertension, and coronary heart disease constitute a phenotype common to individuals with either the IR syndrome or NAFLD1-12. Furthermore, the hepatic steatosis, fibrosis, and cirrhosis characteristic of NAFLD are also frequent histologic findings in patients with IR 3-7. Together, these data beg the question whether NAFLD and IR are causally associated. Support for this notion derives from recent observations that IR may be a strong, independent predictor of NAFLD, even in the absence of glucose intolerance 13. Moreover, since NAFLD has been reported to occur in lean subjects BMI greater than 25 with normoglycemia 14, 15, it is reasonable to postulate that NAFLD may be an early manifestation and a consequence of IR. Increased oxidative stress is an important pathogenic mechanism of obesity-associated metabolic syndrome 16. Fat accumulation correlated with systemic oxidative stress in humans and mice. However, increase oxidative stress as an instigator of the metabolic syndrome in patients with NAFLD as compared to controls has not yet been investigated. Furthermore, impaired cytokine medicated inflammatory response has been shown to correlate with body mass index across the broad range of obesity and may mediate hepatic steatosis andor lead to mitochondrial dysfunction in hepatocytes 17, 18. Discerning whether NAFLD is attributable to increased oxidative stress andor abnormalities in innate immune response would be imperative in identifying potentially useful therapeutic targets for obesity-associated liver disease. 