Several studies have investigated the role of oxidative stress as an important factor in the pathology of metabolic conditions such as NAFLD.9,10 According to the “multiple-hit hypothesis”, lipid accumulation in hepatocytes leads to disruption of the mitochondrial antioxidant capacity as well as endoplasmic reticulum stress, exciting fat oxidation pathways.11 Oxidative stress causes an inflammatory response through the positive regulation of highly sensitive C-reactive protein (hs-CRP), proinflammatory cytokines such as interleukin-6 (IL-6), and tumor necrosis factor α (TNF-α).12,13. This evidence concerns the gene TNF and metabolic dysfunction-associated steatotic liver disease.