Another key point of this model is the addition of fructose, a monosaccharide that is abundant in many processed foods, which is considered to be a major dietary contributor to the pathogenesis of NAFLD, by increasing de novo lipogenesis in hepatocytes, and upregulating tumor necrosis factor (TNF)-α, independently of insulin stimulation [25, 26]. The gene discussed is INS; the disease is metabolic dysfunction-associated steatotic liver disease.