This process drives the cleavage of pro‐IL‐1β and pro‐IL‐18, as well as gasdermin D‐mediated pyroptotic cell death.[1, 2, 3, 4] Aberrant activation of the NLRP3 inflammasome is implicated in diverse inflammatory pathologies, including atherosclerosis, colitis, gout, autoimmune disorders, sepsis, and type 2 diabetes.[1, 2, 3, 4] Consequently, targeting the NLRP3 inflammasome represents a promising therapeutic strategy for these conditions. Here, NLRP3 is linked to gout.