Rel possesses as N-terminal Rel homology domain (RHD), characteristic of NFκB transcription factors, and a C-terminal IκB-like domain. In unstimulated cells, Rel is auto-inhibited - sequestered in the cytosol. Activation of the Imd pathway leads to the cleavage of Rel, releasing the C-terminal IκB domain and allowing translocation of the active, RHD-containing N-terminal portion into the nucleus to regulate transcription of target genes. (Adapted from FBrf0233452.)