In response to reports that the pharmacological inhibition of kynurenine 3-monooxygenase (KMO), and, separately, the transcriptional blockage of the Kmo gene, reduces 3-hydroxykynurenine formation and protects against secondary AKI, Zheng et al., investigated whether mice lacking functional KMO (Kmonull mice) are protected from AKI experimentally induced by the direct induction of renal IRI [95]. The gene discussed is KMO; the disease is acute kidney injury.