Besides immune‐mediated destruction and impaired platelet production, patients with active ITP (vs remission or non‐ITP controls) show evidence of significantly higher expression of NLRP3 inflammasome, adaptor protein ASC, and plasma IL‐18 levels, and increased caspase‐1 activity and markers of endothelial cell activation and neutrophil extracellular trap formation [25, 26]. This evidence concerns the gene IL18 and autoimmune thrombocytopenic purpura.