However, the validity of some animal models has been questioned: The use of a methionine- and choline-deficient diet and/or genetic models, including mutations or knockout of key genes for the regulation of eating behavior such as the leptin or leptin receptor gene, can rapidly induce liver inflammation, but these nonphysiological interventions result in the loss of important aspects of NAFLD pathogenesis (51, 52). This evidence concerns the gene LEP and metabolic dysfunction-associated steatotic liver disease.