Animal study showed that estrogen activated antioxidant enzymes such as Sod2/Gpx1 through modulation of the signaling pathway consisting of the estrogen receptor alpha and peroxisome proliferator-activated receptor-gamma coactivator 1 alpha, and inhibited mitochondrial oxidative damage and inflammatory responses, resulting in female mice being more insensitive to high fat/high fructose diet-induced NAFLD (30), which partly explains the mechanisms underlying the sex-specific role of dietary components on the risk of developing NAFLD. The gene discussed is GPX1; the disease is metabolic dysfunction-associated steatotic liver disease.