Although circulating Ang II protein levels are unchanged in IBD, a marked increase is found within the inflamed bowel,10 where Ang II concentrations correlate with endoscopically graded bowel inflammation.19 This local production of Ang II may be driven by upregulated cathepsin G,25 released by neutrophils,6 which cleaves Agt and Ang I to form Ang II,27 though renin and angiotensin converting enzyme (ACE) are also present in abundance in the intestine. Here, AGT is linked to inflammatory bowel disease.