In particular, LXR-dependent upregulation of SREBP1c potentially limits the usefulness of LXR agonists to improve cholesterol metabolism, as the resulting induction of lipogenic programs could lead to undesirable effects, such as nonalcoholic fatty liver disease (NAFLD), a condition that has risen to epidemic proportions in recent years (20). This evidence concerns the gene SREBF1 and metabolic dysfunction-associated steatotic liver disease.