Indeed, high fish oil diet did not elicit hepatic insulin resistance as shown by the determination of insulin-stimulated AKT phosphorylation (at Ser473), but it induced a lower degree of hepatic steatosis compared to the high lard diet, possibly through an ameliorated mitochondrial utilization of lipid substrates mediated by PPARα and associated with shift towards fusion phenotype. The gene discussed is AKT1; the disease is Insulin resistance.