Rh-ES is an endogenous broad-spectrum angiogenesis inhibitor, which could inhibit VEGF, cyclin D1, metalloproteinases, c-myc, integrins, and even Wnt signaling, thus inhibiting endothelial cell proliferation and migration, suppressing tumor vascularization and blocking the nutrition and oxygen supply to tumor cells [26–28]. The gene discussed is VEGFA; the disease is neoplasm.