Further investigations have demonstrated that FXR acts as a tumor suppressor by inhibiting HCC growth through the disruption of multiple oncogenic signaling pathways, including NF-κB, STAT3, and wnt/β-catenin pathways [58,59,60], or by functioning as a transcription factor that upregulates the expression of p21, a tumor suppressor, thereby impeding HCC cell proliferation [61]. This evidence concerns the gene STAT3 and neoplasm.