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]. This evidence concerns the gene NLRP3 and familial cold autoinflammatory syndrome.