NFKB1 and inflammatory bowel disease: IEC-specific deletion of either NF-κB subunits or components of the upstream IKK (IκB kinase) complex, but also constitutively elevated IKK/NF-κB activity in the intestinal epithelium, consistently resulted in local infiltration of immune cells and inflammation (such as in inflammatory bowel disease), increased IEC apoptosis and tissue damage (Chen et al., 2003; Greten et al., 2004; Nenci et al., 2007; Steinbrecher et al., 2008; Guma et al., 2011; Vlantis et al., 2011; Shaked et al., 2012; Schwitalla et al., 2013; Vereecke et al., 2014; Vlantis et al., 2016; Mikuda et al., 2020).