Rel B is part of the NFκB complex and forms heterodimeric complexes with p50 (NFKB1) and p52 (NFKB2). The homodimeric complexes of Rel B alone do not show DNA-binding activity. IHC analysis has shown that Rel B expression correlated with dendritic cell activation. NFκB-inducing kinase NIK is required for osteoclastogenesis in response to pathologic stimuli and overexpression of Rel B rescues differentiation of mouse NIK -/- osteoclast precursors. Rel B is required for RANKL-induced osteoclastogenesis in vitro and for TNF -induced bone resorption in vivo. This indicates that the alternative NFκB pathway, via Rel B, plays an essential and unique role in RANKL signaling toward osteoclast development.