showed that NSCLC-acquired resistance to TRAIL was arbitrated by NF-κB up-regulation; however, they also observed that p53-independent apoptosis by attenuating NF-κB expression and concurrently suppressing Bcl-2 and Bcl-xL activities in NSCLC, may be responsible for TRAIL-induced apoptosis upon combination therapy with TRAIL and other anti-tumor agents (52). The gene discussed is BCL2L1; the disease is neoplasm.