Furthermore, a few large multicenter case-control studies demonstrate a role of genetic variants implicated in insulin signalling [9], oxidative stress [10, 11], and fibrogenesis [12] in the progression of NAFLD towards fibrosing NASH, and confirm that hepatocellular fat accumulation and insulin resistance are key operative mechanisms in the pathophysiology of NAFLD, and are closely involved in the progression of liver damage. The gene discussed is INS; the disease is metabolic dysfunction-associated steatohepatitis.