Further functional evidence using recombinant kallistatin or adenovirus-mediated kallistatin overexpression in human gastric cancer cells confirms the direct anti-lymphangiogenic effects of kallistatin through binding to LRP6 and inhibiting the IKK/IκB/NF-κB signaling, consequently downregulating VEGF-C expression and secretion (103, 105, 106). This evidence concerns the gene SERPINA4 and gastric cancer.