Either excess generation of peroxisome proliferator-activated receptor-γ (PPAR-γ) or underexpression of hepatocyte apoptosis participates in increasing the sensitivity of insulin [19], which could be achieved by regular improvement of NAFLD via reduced content of lipids in the liver and increased aliphatic acid β-oxidation [19, 25]. Here, INS is linked to metabolic dysfunction-associated steatotic liver disease.