NF-κB signaling pathway can be activated by chemotherapeutic agents and RT, respectively8, 9, followed by the increased expressions of downstream effector proteins, such as cyclin D1, B-cell lymphoma 2 (Bcl-2), tumor necrosis factor (TNF-α), vascular endothelial growth factor (VEGF), X-linked inhibitor of apoptosis protein (XIAP), matrix metalloproteinase 9 (MMP-9), and cyclooxygenase-2 (COX-2), and results in the tumor proliferation, anti-apoptosis, invasiveness and radioresistance9. The gene discussed is NFKB1; the disease is neoplasm.