Herein, our findings showed the following: (1) burn-induced renal inflammation contributes to the development of early AKI, with a concurrent increase in oxidative stress; (2) the TLR4/NF-κB pathway is involved in regulation of renal inflammation after burn insult and is dependent on MyD88; (3) ATX dose-relatedly attenuates activation of the TLR4/MyD88/NF-κB cascade and the subsequent release of inflammatory mediators; and (4) ATX further upregulates renal expression of HO-1 in a dose-related manner to assist in its regulation of oxidative stress and the TLR4 pathway. The gene discussed is MYD88; the disease is acute kidney injury.