Both neutrophil elastase and cathepsin G have been shown to cleave and activate IL-1β, albeit to a lesser extent than caspase-1, yet disease progression of neutrophil-dominated forms of arthritis in Casp1−/− is comparable to that in wild type mice, suggesting a functional role for other enzymes in the regulation of IL-1β24, 25, 26. The gene discussed is IL1B; the disease is arthritic joint disease.