The inhibition of the NLRP3 inflammasome by inhibitors or genetic deletion of NLRP3 can ameliorate renal diseases (1–3).Activation of NLRP3 after priming requires the secondary signals such as NLRP3 relocalization to mitochondria, production of mitochondrial reactive oxygen species (ROS), K+ efflux, and cathepsin release from lysosomal membranes (4–6). This evidence concerns the gene NLRP3 and kidney disorder.