Pro-inflammatory diets may genetically interfere with hepatic β-oxidation, resulting in a massive upregulation of pro-inflammatory molecules (e.g., IL-1β, IL-17, and IL-18) and oxygen-responsive substances, which in turn increases the production of endogenous lipids and increases the risk of NAFLD, as well as exacerbating the damage related to chronic disease (1, 29, 30). This evidence concerns the gene IL1B and metabolic dysfunction-associated steatotic liver disease.