Inflammasome activation and subsequent caspase-1-dependent IL-18 maturation have been implicated in SLE pathogenesis, with studies demonstrating heightened caspase-1 activity in peripheral blood monocytes of SLE patients and an increased expression of inflammasome components, including NLR family pyrin domain containing 3 (NLRP3) and caspase-1 in LN biopsies.22 23 Caspase-1 inhibition could inhibit the activation of IL-18 and alleviate LN. This evidence concerns the gene IL18 and lobular neoplasia.