The intensity and maintenance of the inflammatory response, both in clinical and experimental IBD, are also determined by coordinated mechanisms of cell recruitment, which comprise the positive regulation of the expression of intercellular adhesion molecules (ICAM-1) and chemokines (MIP-2 and MCP-1), mainly by activated NF-κB p65 (Trzeciak-Jędrzejczyk et al., 2017; Wang et al., 2018). The gene discussed is NFKB1; the disease is inflammatory bowel disease.