The inflammatory microenvironment of SLE patients increases NF-κB expression in glomerular endothelial and mesangial cells, while NF-κB overexpression can induce the expression of inflammatory cytokines, chemokines, adhesion molecules, and inflammatory enzymes, creating a vicious cycle (Liu et al., 2019). Here, NFKB1 is linked to systemic lupus erythematosus.