Moreover, the core targets were predominantly related to several KEGG pathways, such as apoptosis-related, liver disease (NAFLD, hepatitis B and hepatocellular carcinoma)-related, TNF, VEGF, NF-κB, and MAPK pathways (Figure 4B), implicating their involvement in the effects of SNS on liver fibrosis. This evidence concerns the gene TNF and metabolic dysfunction-associated steatotic liver disease.