Our studies indicate that the ablation or inhibition of SMOX and SAT1, as well as neutralization of the products of their enzymatic activity (e.g., H2O2 and reactive aldehydes), reduce the severity of endotoxin-, I/R-, and cisplatin-induced AKI by dampening the severity of oxidative stress, the inflammatory/innate immune response, and the ERS/UPR response [7,47]. This evidence concerns the gene SAT1 and acute kidney injury.