In addition to the recognized functions of this pathway, including the regulation of lymphoid organ development, B cell survival, and maturation [36,37], an important role in regulating DC development and maturation has been reported using mice deficient in NF-B members RELB, cREL, or both cREL and NF-B1, noting that DCs require RELB to induce T cell responses via both the conventional antigen-presenting pathway and via cross-priming [38,39,40], which implies an essential role in the anti-tumor immune response [41]. The gene discussed is RELB; the disease is neoplasm.