In contrast to extra-intestinal tissues, ADAMDEC1 has been identified as significantly under-expressed in a number of diseases that affect the gut, such as GI cancers and Crohn’s disease.7–9,11,12 This phenomenon is unlikely to be secondary to bowel inflammation per se, as we have clearly shown that Adamdec1 is significantly upregulated, at a tissue level, in the bowel of mice following exposure to a colitogenic agent and induction of an acute colitis. The gene discussed is ADAMDEC1; the disease is colitis.