In the process of radiotherapy or chemotherapy, NF-κB in tumor cells will be further activated due to the damage of drug toxicity and side effects; high-activity NF-κB can promote the massive production of anti-apoptotic factors, such as Bcl-xL, Bcl-2, IAPs, XIAP, and survivin, and inhibit cancer cell apoptosis, resulting in drug resistance [32]. This evidence concerns the gene BCL2 and neoplasm.