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. Here, NR1I2 is linked to metabolic dysfunction-associated steatotic liver disease.