IR plays a major role in the development of NAFLD by promoting hepatic lipogenesis (due to hyperinsulinaemia, as this pathway retains its sensitivity to insulin) and impairing the inhibition of adipose tissue lipolysis, subsequently leading to the accumulation of fats in the liver mainly as triglycerides, resulting in NAFL. The gene discussed is INS; the disease is metabolic dysfunction-associated steatotic liver disease.