Tumor necrosis factor-like weak inducer of apoptosis (TWEAK), which promotes inflammation via NFκB/STAT3 pathways, may also play a major role in the long-term outcome of AKI by activating fibroblast growth factor-inducible-14 (Fn14) receptor, as has been reviewed recently (98). This evidence concerns the gene NFKB1 and acute kidney injury.