Ma and colleagues recently showed that BRD4 is aberrantly activated in the inflamed colon of IBD patients and ZL0516, an oral BRD4 BD1 inhibitor, reduced TNFα- and LPS-induced production of inflammatory cytokines in human colonic epithelial cells and peripheral blood mononuclear cells, and both prevented and cured experimental colitides in mice as a result of its ability to block the activation of the BRD4/NF-κB signaling pathway (Ma et al., 2025). Here, NFKB1 is linked to inflammatory bowel disease.