NASH and related liver fibrosis are largely caused by these metabolic disorders, our studies that the recovering effects of JT003 on the HFD induced NASH and CCl4 induced liver fibrosis involved the amelioration on insulin resistance, PI3K-Akt signals, HSCs activation as well as ER-mitochondrial axis function (Fig. 8k). The gene discussed is AKT1; the disease is metabolic dysfunction-associated steatohepatitis.