Given the important roles of oxidative stress and secondary renal inflammation in severe burn-induced early AKI, we hypothesized a possible role of ATX in protection via its anti-inflammatory effects and the potential mechanisms of action in early postburn AKI through the regulation of the TLR4/NF-κB pathway and HO-1, we and aimed to explore more details to support clinical treatment. The gene discussed is NFKB1; the disease is acute kidney injury.