It has recently been suggested that hepatocellular injury in NAFLD may be attributable to the combined effects of severe peripheral insulin resistance and relative failure of humoral (adipokine) mediators that combat the effect of high insulin levels on hepatic lipid turnover.25 However, ALT levels increased already within a week, a time period after which a significant increase of lipids within hepatocytes seems unlikely to have developed. The gene discussed is INS; the disease is metabolic dysfunction-associated steatotic liver disease.