In neutrophils, caspase-1 mediates IL-18 release independent of NLRP3 activity, suggesting that caspase-1 activity in neutrophils during RA is mediated by other inflammasomes or through the action of neutrophil proteolytic enzymes, such as metalloproteases, serine proteases and cathepsins, that may activate caspase-1 [198]. The gene discussed is CASP1; the disease is rheumatoid arthritis.