Wang et al. found that IL-22 ameliorated renal injury and fibrosis in diabetic nephropathy via downregulating renal NLRP3/caspase-1/IL-1β pathway in a mouse model [18], while Weber et al. reported that inhibition of the biological activity of IL-22 by IL-22-binding protein improved host defense and alleviated acute polymicrobial peritonitis-mediated kidney failure [19]. This evidence concerns the gene NLRP3 and diabetic kidney disease.