The authors have hypothesised that reduced ACE2 activity predisposes to inflammation and mural fibrosis in IBD probably through three mechanisms: i) reduced angiotensin (5–6–9–12–27); ii) tryptophan deficiency (26) and iii) elevated levels of serine-protease, the essential primer that can activate the S protein, was reportedly 10 times higher in IBD than in healthy subjects (28). This evidence concerns the gene ACE2 and inflammatory bowel disease.