Research has found that inhibition of NLRP3 inflammasome via receptor-interacting protein kinase 3 (RIP3) would lead to the amelioration of LN and the decline of auto-antibody production (56), which suggests that various signaling pathways for the activation of NLRP3 inflammasome are operative in the pathogenesis of lupus and targeting LRGs might work with LN via NLRP3. The gene discussed is NLRP3; the disease is systemic lupus erythematosus.