Patients with obesity and IBD are prone to a TNF-sink phenomenon where TNF- α blockers are sequestered within the adipose tissue-secreted TNF-a; high body weight appears to be a risk factor for increased drug clearance, resulting in short half-life and low trough drug concentrations as shown in population pharmacokinetics studies involving IBD-approved biological therapies such anti-TNFa and anti-integrins [58]. This evidence concerns the gene TNF and inflammatory bowel disease.