Therefore, this study aims to clarify the contribution of JNK/Sab signaling-mediated mitochondrial dysfunction to NASH, then to explore the role of scoparone against NASH and whether the JNK/Sab signaling pathway-mediated lipotoxic injury in hepatocytes is involved in its underlying mechanism through in vivo and in vitro experiments. The gene discussed is SH3BP5; the disease is metabolic dysfunction-associated steatohepatitis.