FXR acts as a tumor suppressor in HCC possibly through the following mechanisms: (1) the suppression of ROX generation, thereby decreasing the risk of DNA damage and genomic instability; (2) the upregulation of its downstream tumor suppressors; (3) reducing liver inflammation and fibrosis by the upregulation of fibrosis-promoting proteins such as collagen, TNF-α, IL-1β, IL-6, MMPs, tissue inhibitor of metalloproteinases 2 (TIMP-2), and transforming growth factor (TGF)-β1; (4), maintaining the normal liver metabolism of BAs, glucose, and lipids [83,84,85]. The gene discussed is IL6; the disease is neoplasm.