However, certain genetic animal models, such asob/ob (leptin) mice ordb/db (leptin receptor) mice can exhibit obesity phenotypes,15,16 but do not reflect the etiology of obesity and related diseases as well as in humans as effectively.17 Preclinical models of NASH are designed to mimic the same factors that trigger human disease, one of which is related to excessive calorie consumption. This evidence concerns the gene LEP and metabolic dysfunction-associated steatohepatitis.