In conclusion, fimasartan may ameliorate NAFLD mainly through the activation of oxidative metabolism represented by PPARδ-AMPK-PGC-1α pathway, and its effect may be additionally derived from the inhibition of fatty acid synthesis (11β-HSDH1, FAS, and ACC) and inflammation (TNFα), also the elevation of fatty acid oxidation (MCD and MCAD) and adiponectin level (Figure 8). The gene discussed is PPARGC1A; the disease is metabolic dysfunction-associated steatotic liver disease.