In a human IBD model, which is characterised by increased histone deacetylases (HDACs), nuclear factor-κB (NF-κB), nuclear factor kappa-B kinase β (IKKβ), TNF-α, NOD2, and toll-like receptor (TLR) upregulation have been reported to occur in the inflamed IECs, resulting in high pro-inflammatory cytokine expression levels [56]. This evidence concerns the gene NFKB1 and inflammatory bowel disease.