Although controversial results have been reported with regard to changes in SOD activity observed in NAFLD models [32,33], our results are in good accordance with those shown in a rat model of insulin resistance induced by a high-fat diet, where the over-expression of mitochondrial SOD played a central role in counteracting the redox imbalance and protecting against the insulin resistance set off by the diet in rat skeletal muscle [34]. The gene discussed is SOD1; the disease is Insulin resistance.