➢ Eliminate specific microbial populations that contribute to hyperinflammatory states to modulate IBD severity/disease activity➢ Prevent overgrowth of harmful microbial species that may lead to secondary IBD complications (e.g. pouchitis and abscesses)➢ Influence the development of anti-drug antibodies that affect the risk of immunogenicity to anti-TNF biologics➢ Increase risk of microbial resistance➢ Increase risk of infections (e.g. Clostridium difficile). This evidence concerns the gene TNF and inflammatory bowel disease.