Since antiphospholipid antibodies (aPL) can induce NLRP3 and caspase-1 activation, leading to inflammasome assembly and, via IL-1β and IL-18, promoting inflammation, oxidative stress and endothelial dysfunction,48 49 another potential application of caspase-1 inhibition is in antiphospholipid syndrome (APS), particularly in microvascular manifestations such as aPL-associated nephropathy. This evidence concerns the gene IL18 and autoimmune polyendocrinopathy.