Subsequent studies on peripheral blood mononuclear cells (PBMCs) of APLAID patients suggested that the S707Y mutation of PLCG2 contributes to the activation of the NOD-like receptor (NLR) family, pyrin domain–containing protein 3 (NLRP3) inflammasome in these patients, presumably by promoting, through increased [Ca2+]i, inflammasome component assembly and spontaneous inflammasome activity [14, 15]. This evidence concerns the gene PLCG2 and autoinflammation-PLCG2-associated antibody deficiency-immune dysregulation.