SIX1 suppressed the expression of epithelial marker E-cadherin by activating TGF-β, which promoted EMT and finally resulted in tumor metastasis.[57] In addition, SIX1 promoted lymphanogenesis by upregulating vascular endothelial growth factor (VEGF)-C to contribute to tumor metastasis.[57,58] However, tumor metastasis was regulated by a complex network. The gene discussed is VEGFC; the disease is neoplasm.