RelB is a member of the NFkB family which also includes p50 (NFkB1), RelA (p65), p52 (NFkB2), and c-Rel. Functionally, RelB and can act as either an activator or repressor of transcription by forming heterodimers with the p50 and p52 NFkB family members. Stabilization of RelB is believed to require the presence of p100/p52 and p105/50. Although RelB knock out mice are viable, there are complex abnormalities in their inflammatory response, hematopoietic lineage and formation of secondary lymphoid structures. RelB is known to cross talk with aryl hydrocarbon receptor (AhR) signaling pathways, possibly contributing to the inflammatory response.