This mechanism leads to an increase of hepatic cholesterol synthesis and activation of pro-apoptotic genes (p53 and P66SHC), which contributes to oxidative stress and apoptosis due to reduced β-oxidation resulting in restoration of nicotinamide phosphoribosyltransferase/nicotinamide-adenine-dinucleotide (NAMPT/NAD+) levels and therefore ameliorates hepatic steatosis and inflammation [86,88,90,91]. The gene discussed is NAMPT; the disease is fatty liver disease.