Increased plasma levels of 3-hydroxykynurenine in AP patients paralleled disease severity in clinical AP [64], while inhibition of kynurenine-3-monooxygenase, an enzyme downstream of IDO, prevented multiple organ failure in rodent AP models [18]; a series of kynurenine-3-monooxygenase inhibitors is now in development for AP therapy [17]. The gene discussed is KMO; the disease is alkaline phosphatase measurement.