AMPK also phosphorylates SREBP-1c, which inhibits proteolytic maturation, nuclear translocation of SREBP-1c, and the expression of the downstream fatty acid synthase gene, thus increasing fatty acid β-oxidation and reducing the de novo synthesis of triglycerides (TG) [33] and their liver accumulation, finally preventing hepatocyte steatosis [34] (Figure 1). The gene discussed is SREBF1; the disease is steatosis.