AGER and colitis: Soluble RAGE acts as a decoy receptor for RAGE, binding to the same damage-induced ligands as membrane-bound RAGE, but because it lacks a cytoplasmic tail, it cannot initiate pro-inflammatory signalling.26 Thus, higher levels of sRAGE might block inflammation, and reduced levels of sRAGE have been found in mice with chronic inflammation and in patients with chronic inflammatory diseases.22 Reduced epithelial RAGE expression followed by increased sRAGE in colitis-resistant mice suggests shedding of RAGE as a protective response against the development of chronic inflammation.