An accepted concept of NAFLD pathogenesis involved a “2-hit” process, in which the abnormal metabolic environment is causing lipid accumulation comprised of the “first hit,” and this hit increases the susceptibility of the liver to secondary injuries (“second hit”) in inflammation.6 The severe consequences include mitochondrial dysfunction, overproduction, and the release of proinflammatory cytokines and chemokines, which notably include macrophage chemotactic protein 1, tumor necrosis factor α (TNF-α), interleukin (IL) 1β, and IL-1.7 This evidence concerns the gene TNF and metabolic dysfunction-associated steatotic liver disease.