USP16 and inflammatory bowel disease: Under lipopolysaccharide or TNF-α stimulation, competing with NEMO, USP16 specifically deubiquitinates the Lys33-linked polyubiquitination of IKKs and promotes IKK-β-mediated p105 phosphorylation without direct IκBα or p65 phosphorylation, leading to an autoimmune response and IBD colon cancer progression [40].