A particularly strong example of this was an elegant study in a mouse model that conclusively showed: (1) NLRP3 inflammasome activation to be the primary factor underlying progressive renal failure caused by oxalate nephropathy; and (2) oxalate nephropathy-associated renal failure was due to NLRP3-mediated inflammation and not any effect on oxalate intestinal handling, metabolism rate, or general oxalate homeostasis [117]. This evidence concerns the gene NLRP3 and acute kidney injury.