These cells release a range of circulating inflammatory proteins (CIPs), such as tumor necrosis factor-alpha (TNF-α), interleukin-1β (IL-1β), interleukin-6 (IL-6), and interleukin-18 (IL-18), which initiate and amplify the inflammatory cascade that underpins the pathogenesis of gout.[3,4] Among these, the interleukin-1(IL-1) family of cytokines is particularly critical, playing a pivotal role in both innate immunity and the regulation of inflammatory processes. The gene discussed is IL1B; the disease is gout.