Despite the well-known concept that extraintestinal inflammatory diseases (i.e., AS, JIA, psoriasis, and PsA) can represent independent risk factors for the development of IBD, the fact that, after the interruption of ETA and the switch to a different anti-TNF-α or the swap to another biological agent, patients usually obtain an immediate improvement of gastrointestinal inflammation suggests the theory of a paradoxical effect [101,102]. The gene discussed is TNF; the disease is juvenile idiopathic arthritis.