Specifically, in the context of NAFLD, the lipid accumulation in hepatocytes (hepatic macro-vesicular steatosis), driven by increased fat intake, occurs and increases the vulnerability of the liver to a variety of secondary insults such as oxidative stress, and the subsequent activation of inflammatory pathways by the production of pro-inflammatory cytokines, including IL-1, IL-6, and TNF-α through toll-like receptor 4 activation, by Kupffer cells or adipokines from adipocytes, dysregulated hepatocyte apoptosis and hepatic stellate cell activation. This evidence concerns the gene TNF and metabolic dysfunction-associated steatotic liver disease.