In particular, the activation of the NLR family pyrin domain containing 3 (NLRP3) inflammasome usually leads to the release of proinflammatory cytokines such as IL-1β and IL-18.4 Furthermore, recent studies have identified the inhibition of NLRP3 inflammasome formation as a potential therapeutic target for mitigating gout development.5 The NLRP3 inflammasome is implicated not only in the activation of the NF-κB signaling pathway but also in apoptosis. Here, IL1B is linked to gout.