The activity of these SLs is mainly attributed in part to their ability to target cell surface transferrin receptors (a distinct hallmark of rapidly proliferating cells), NF-κB signaling (by disrupting the recruitment of IκB kinase complex to the TNF receptor, which is essential for tumor initiation, progression and resistance), and the angiogenesis pathways, by inhibiting human vein endothelial cell proliferation and vascular endothelial growth factor and receptor expression [57, 58]. The gene discussed is VEGFA; the disease is neoplasm.