In the HBV-induced hepatitis model, out of 217 pathways modulated, nine pathways—namely, PI3K-Akt, TNF, JAK-STAT, MAPK, Chemokine, NF-kappa B, TGF-beta signaling pathways, Apoptosis, and Cell cycle—were prioritized to compare with chemically-induced hepatitis, as these pathways were significantly associated with the progression of hepatocellular carcinoma induced by HBV (refer KEGG ID: hsa05161). Here, SOAT1 is linked to hepatitis A virus infection.