TEAD inhibitors (estrogen receptor, ER) significantly altered metabolic pathways, such as AMPK and PI3K/AKT signaling and reduced the expression of lipid metabolism related genes such as SREBP1 and 3-hydroxy-3-methylglutaryl-Coenzyme A reductase (HMGCR) (responsible for controlling cholesterol synthesis) by directly binding to their promoters to alleviate hepatic steatosis in HFD-induced MASLD male mice [13]. The gene discussed is HMGCR; the disease is fatty liver disease.