Previous inquiries have elucidated that the Toll-like receptor 4 (TLR4)/nuclear factor-κB (NF-κB) signaling pathway constitutes a critical nexus mediating inflammation and is accountable for the initiation of mitochondrial dysfunction (55), recognized as one of the signaling pathways implicated in the onset of SA-AKI (56–58). This evidence concerns the gene NFKB1 and acute kidney injury.