Out of many downstream effects of AMPK activation, the most important in MASLD are inhibition of ACC, which promotes ß-oxidation; inhibition of sterol regulatory element-binding protein 1 (SREBP-1c), which downregulates fatty acid synthase (FAS) and de novo lipogenesis; and inhibition of β-Hydroxy β-methylglutaryl-CoA (HMG-CoA) reductase, which reduces cholesterol synthesis and promotion of glucose transporter 1 and 4 translocation towards cell membranes. Here, SREBF1 is linked to metabolic dysfunction-associated steatotic liver disease.