FAS and metabolic dysfunction-associated steatotic liver disease: For instance, GSK2033 could significantly improve rather than suppress the expression of the lipogenic genes such as FAS and SREBP‐1c and therefore had no effect on hepatic steatosis in a mouse model of non‐alcoholic fatty liver disease.41 Furthermore, these antagonists may target a number of other nuclear receptors, such as the glucocorticoid receptor, pregnane X receptor and farnesoid X receptor, all of which can definitely alter hepatic gene expression.41 However, the underlying mechanisms of these antagonists on lipid metabolism need to be further investigated.