We went on to show that this protection from lipid-induced hepatic insulin resistance was associated with marked reductions in hepatic DAG content, decreased hepatic PKCε activity, and increased insulin-stimulated Akt phosphorylation, consistent with previous studies in humans and animals implicating a causal role of DAG-mediated PKCε activation in mediating hepatic insulin resistance.1 Finally, in order to examine if these results translate to humans, we found that hepatic PNPLA3 expression was positively correlated with hepatic DAG content and insulin resistance in humans. The gene discussed is AKT1; the disease is Insulin resistance.