In this review, we will focus, in particular, on three examples: Cryopyrin-Associated Periodic Syndrome, an autoinflammatory diseases associated with excessive release of IL-1β, due to constitutive activation of the NLRP3 inflammasome platform; Mevalonate Kinase Deficiency, in which increased release of IL-1β is the indirect result of a metabolic defect involving the biosynthesis of sterols; and interferonopathies, which are monogenic disorders similar to Systemic Lupus Erythematosus, in which excessive levels of Type I IFNs are the main mediator of inflammation. This evidence concerns the gene NLRP3 and cryopyrin-associated periodic syndrome.