Collectively, these findings reveal a paradoxical duality of the NLRP3 inflammasome in autoimmunity: Basal, homeostatic NLRP3 activity may be essential for immune tolerance and suppression of aberrant lymphocyte activation; however, sustained or excessive NLRP3 inflammasome activation drives cytokine storm, immune dysregulation, and target organ damage—thereby fueling LN progression. This evidence concerns the gene NLRP3 and Autoimmunity.