The experimental model we selected was a non-obesogenic, nutrient-deficient, high-fat diet model (Table S1), which offers the advantages of a rapid onset of disease and mirrors the complexity of clinical NASH with fibrosis and development of tumors [15,16,21] but obviates the influence of weight gain [15] and peripheral insulin resistance [22,23]. The gene discussed is INS; the disease is metabolic dysfunction-associated steatohepatitis.