A recently published study found that atypical NF-κB2 signaling amplifies RelA activity in colonic epithelial cells, increases RelA-driven inflammatory gene expression, and exacerbates intestinal pathogenesis in IBD patients and mice with colitis, suggesting that the atypical NF-κB2 pathway may be a potential therapeutic target for inflammatory diseases (Chawla et al., 2021). This evidence concerns the gene NFKB2 and colitis.