A potential mechanism for increased thromboinflammation in diabetes is increased activity of transcription factor NF‐κB (nuclear factor kappa B) and upregulation of genes encoding for several inflammatory markers, including IL‐6 (interleukin 6) and TNF‐α (tumor necrosis factor alpha), as observed in cultured murine cerebral endothelial cells under hyperglycemic conditions25 (Table 1). The gene discussed is IL6; the disease is diabetes mellitus.