Indeed, our Cth–/– mice displayed the systemic resistance against caerulein-induced acute pancreatitis [24], cecal-ligation and puncture-induced sepsis [25], and acute renal ischemia/reperfusion injury and its associated inflammatory responses [26], suggesting the pro-inflammatory roles of endogenous H2S produced by CTH at those inflammation loci. The gene discussed is CTH; the disease is acute pancreatitis.