In addition, increased IL1B expressions in the kidneys of 191 patients with CKD were inversely correlated with the glomerular filtration rate (GFR) (Figure 1B), suggesting that IL1B secretion, activities of CASP1-inflammasome, and CASP4/11-noncanonical inflammasome may be increased in CKD and are similar to the cleavage of CASP1 and CASP11 reported in the rat model of hyperuricemic nephropathy (25), roles of NLRP3 inflammasome in various kidney diseases (26), and animal models of kidney diseases (27). This evidence concerns the gene IL1B and chronic kidney disease.