Literature reveals variable results about alteration in leptin [159–161], adiponectin, and TNF-α [153, 162] while the role of resistin in NAFLD in humans still awaits to be examined [162–164] though increased resistin levels have been correlated with NAFLD severity and NASH development [165, 166]. The gene discussed is TNF; the disease is metabolic dysfunction-associated steatotic liver disease.