Thus, renal TNFα is proposed to be responsible for some of the renal dysfunction observed in LPS-induced AKI [6]; [14] through both direct cellular injury [15] and the amplified induction of localized inflammatory mediators (via NFκB activation), including cytokines and chemokines which stimulate the infiltration of damaging neutrophils and monocytes into the kidneys, particularly the renal cortex [6]. This evidence concerns the gene NFKB1 and acute kidney injury.