It induces phase II carcinogen-metabolizing enzymes, inhibits prenyl-transferase activity, increases cell autophagy (via MAP1LC3B, mitochondrial death pathway, the PI3k/Akt pathway, and caspase-3 and -9 activity) and differentiation, reduces cyclin-D1 and increases TGF-β signaling, decreases tumor-induced immunosuppression, reduces circulating Vascular Endothelial Growth Factor (VEGF) and blocks the receptor VEGF-R1, increases DNA damage repair and PARP cleavage. It modulates the expression of the chemotactic protein MCP-1 and of the proteolytic enzymes MMP-2, MMP-9. The gene discussed is FLT1; the disease is neoplasm.