Treatment with quercetin (Table 4) was able to attenuate all these metabolic disorders, while these effects were attenuated by the administration of compound C. Oral administration of quercetin during a high-cholesterol diet blocked the cholesterol-induced activation of PP2C, promoted the activation of AMPK and subsequently the inactivation of ACC, 3-hydroxy-3-methyl-glutaryl-CoA reductase (HMGCR) and FAS ligand. The gene discussed is PRKAA2; the disease is metabolic disease.