It reduces IL‐1β and IL‐18 production in human monocytes and attenuates caspase‐1 activation and IL‐1β secretion in mouse models of NLRP3‐associated diseases, such as Muckle–Wells syndrome, familial cold autoinflammatory syndrome, and urate crystal‐induced peritonitis. The gene discussed is IL1B; the disease is familial cold autoinflammatory syndrome.