In our study, the involvement of NF-κB in TRAIL-induced resistance of DCHIV is suggested by the recent demonstration of the ability of HMGB1 to increase c-IAP2 expression levels in carcinoma cells by enhancing NF-κB activity [39], and the requirement for HIV to promote its replication and prevent host-cell apoptosis by activating NF-κB [45]. This evidence concerns the gene BIRC3 and carcinoma.