MCs are hypothesized to mediate autoinflammation through NLRP3 inflammasome sensing of extracellular threats; mutations to the NLRP3 inflammasome and its mediators leads to monogenic diseases such as familial Mediterranean fever (FMF) and cryopyrin-associated periodic syndrome (CAPS) which arise from exuberant caspase-1 activity leading to downstream IL-1β secretion and subsequent inflammation [70]. This evidence concerns the gene NLRP3 and cryopyrin-associated periodic syndrome.