In ischemic reperfusion injury (IRI) [48], folic acid-induced nephropathy [49], cisplatin-induced AKI [50], rhabdomyolysis-induced AKI [51], and contrast-induced AKI [52] models, NLRP3-mediated activation of inflammasomes can be detected, and the progression of AKI is mediated through canonical and noncanonical inflammasome pathways. This evidence concerns the gene NLRP3 and Nephropathy.