Many tumours have been reported to show upregulation of a large number of NFκB target genes, for examples, FLICE-like inhibitory protein (FLIP), Inhibitors of Apoptosis (IAPs) and some members of anti-apoptotic Bcl-2 family to inhibit apoptosis; cyclin D1, c-myc and c-myb to enhance cell proliferation; and cell adhesion molecules (ICAM-1, E-selectin), matrix metalloproteinases and several angiogenic factors such as vascular endothelial growth factor (VEGF) to promote cancer cell invasion [27, 30-35]. This evidence concerns the gene NFKB1 and neoplasm.