In contrast, we found that the NAFLD and hepatic insulin resistance could be attributed to increased hepatocellular DAG content and activation of PKCε, which we have previously demonstrated causes decreased insulin signaling at the level of the insulin receptor kinase.20, 30 This finding is in contrast to another recent report of a PNPLA gene variant that was associated with NAFLD but was not associated with insulin resistance.31 Here, PRKCE is linked to metabolic dysfunction-associated steatotic liver disease.