Therapeutic agents targeting IL-1β, such as anakinra, rilonacept, and canakinumab, have been used to treat patients with autoinflammatory diseases, such as CAPS, which involve gain of function mutations of NLRP3; however, IL-1β-targeting biologic agents affect various types of signals from inflammasomes and/or non-specific proteases that result in the accumulation of IL-1β21. This evidence concerns the gene NLRP3 and cryopyrin-associated periodic syndrome.