Our previous study has uncovered the role of complement C1q with its ligand PTX3 in promoting NLRP3 inflammasome over-activation, GSDMD-conferred pyroptosis, and inflammatory cytokine release in RA-derived monocytes [6]. A recent study by Zhai et al. supports the notion of a pathogenic role of GSDME [13]. The gene discussed is NLRP3; the disease is rheumatoid arthritis.