Although the pathogenesis of gout has not been determined, the activation of the NLRP3 inflammasome triggered by uric acid is considered to be a key pathogenic mechanism in the acute inflammatory response of gout, which leads to the production of proinflammatory cytokines, including interleukin-1β (IL-1β) and IL-18 [2,3]. This evidence concerns the gene IL18 and gout.