Familial cold autoinflammatory syndrome (FCAS), Muckle–Wells syndrome (MWS) and neonatal-onset multisystem inflammatory disorder (NOMID, also known as chronic infantile neurologic, cutaneous, and articular (CINCA) syndrome) have been shown to be caused by gain of function mutations in the NLPR3 gene encoding for cryopyrin, leading to increased caspase-1 and IL-1β activity [75,76,77,78]. The gene discussed is IL1B; the disease is familial cold autoinflammatory syndrome.