The clinical significance of our findings were illustrated by our observation that high levels of FADD in the synovial fluids from gout patients were correlated with levels of NLRP3 inflammasome inducer (MSU derived from high uricaemia) and NLRP3 inflammasome activity (IL-1β concentrations), confirming that NLRP3 inflammasome activation might lead to FADD secretion in vivo. The gene discussed is IL1B; the disease is gout.