NLRC4 and autoinflammatory syndrome: Strikingly, in humans, constitutive NLRC4 hyperactivation through mendelian inheritance of various de novo gain-of-function (GOF) mutations results in a broad array of clinical features, including severe enterocolitis and gut inflammation (5–7), leading to autoinflammatory syndromes collectively termed NLRC4 inflammasomopathies (8).