In acute kidney injury, the roles of IL-33 and sST2 are even less clear: in a study of myocardial infarction, elevated sST2 predicted acute kidney injury [54], but murine studies have shown IL-33-dependent endothelial activation, a process that should be dampened by elevated sST2 levels, leading to acute kidney injury after infection [55]. The gene discussed is IL33; the disease is myocardial infarction.