Recently, Ives et al. reported that XOR regulates macrophage IL1b secretion upon NLRP3 inflammasome activation, and febuxostat suppresses the activation by inhibiting XOR-generated ROS production.[12] Febuxostat has also been shown to reduce tissue damage in myocardial dysfunction and chronic kidney disease.[38] Thus, the mechanisms of the beneficial effects of XOR inhibitor treatment are likely to be multi-factorial. This evidence concerns the gene NLRP3 and chronic kidney disease.