This is supported by evidence highlighting caspase-1 as a key mediator of inflammasome dysregulation in SLE.8 31 Elevated caspase-1 activity as a result of increased inflammasome activation in monocytes was observed in SLE patients and correlated with disease severity.22 40 It has already been described inflammasome inhibition by targeting NLRP3 or cyclic GMP-AMP synthase-stimulator of interferon genes (cGAS-STING) pathway had the potential to downregulate caspase-1 activity induced by SLE serum in human monocytes.40 Here, CGAS is linked to systemic lupus erythematosus.