Secondly, we evaluated whether the miRNAs differentially expressed in insulin-resistant HSCs could impact on NAFLD-related fibrosis by using an experimental model of IR-NASH that develops hepatic IR reminiscent of that observed in patients with accumulation of FoxO1 and impairment of glucose metabolism but preserved activation of de novo lipogenesis [8,9]. The gene discussed is INS; the disease is metabolic dysfunction-associated steatotic liver disease.