In addition, CFTR malfunction suffices to increase the production of interleukin-15 (IL15), a pro-inflammatory cytokine critical for CD pathogenesis [29, 32, 33, 35–37], as the result of TGM2-mediated NF-κB activation, exactly as this occurs in CF epithelia [28]. The gene discussed is NFKB1; the disease is cystic fibrosis.