Furthermore, the TLR4-MyD88 (namely Myeloid Differentiation Primary Response 88) axis activated STAT3 (Signal Transducer and Activator of Transcription 3) and SP1 (Specificity Protein 1), which are both transcription factors of the mRNA of the vascular endothelial growth factor (VEGF), so VEGF was overexpressed, which improved HCC angiogenesis and pulmonary metastasis [65]. The gene discussed is STAT3; the disease is hepatocellular carcinoma.