LPS induces the release of inflammatory cytokines (especially TNF-α and IL-1β) through TLR4 signaling pathways and contributes to oxidative stress, which can activate tubular epithelial cells and result in functional damage to these cells, subsequently causing renal microcirculatory disturbance and hypoperfusion, which finally leads to SA-AKI [26–28]. The gene discussed is TLR4; the disease is acute kidney injury.