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Additionally, <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u20101 inhibitors may also help patients with polyarticular and tophaceous gout by making them less vulnerable to breakthrough attacks during initiation of chronic urate\u2010lowering treatment, the mainstay of gout therapy. Because evidence highlights the role of proinflammatory cytokine <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u20101 in the inflammation process during an acute gouty attack, <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u20101 inhibitors are used to modulate the pathogenesis of a variety of autoinflammatory diseases, providing support for its potential role in the inflammatory process of gout. After <jats:styled-content style=\"fixed-case\">NSAID<\/jats:styled-content>s, colchicine, and steroids, <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u20101 inhibitors are beneficial as fourth\u2010line therapy for acute gout attacks due to their high cost and limited clinical experience. The <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u20101 inhibitors used in gout are anakinra, canakinumab, and rilonacept. Based on published evidence, anakinra has limited support in the form of anecdotal case reports to justify its use for treating gout. Canakinumab's toxic profile in clinical trials precludes its use in treating patients for gout, and rilonacept shows promise with a few well\u2010designed studies to support its use in gout patients initiating urate\u2010lowering treatment. 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