These mechanisms include the reduction of ketohexokinase in the liver, resulting in lower fructose uptake and reduced lipogenesis, increased expression of patatin-like phospholipase domain-containing protein 3 (PNPLA 3), which has been associated with a lower incidence of non-alcoholic fatty liver disease (NAFLD), and PPARα agonist activity similar to fibrates [44] [Figure 1]. Here, KHK is linked to metabolic dysfunction-associated steatotic liver disease.