Notably, persistent elevation of urinary 11dhTxB2 post-ASA (Fig 2) likely arises predominantly from hyperglycemia-driven COX-2 upregulation in non-platelet cells (e.g., endothelium, monocytes)---a pathway less sensitive to ASA---and/or rapid resynthesis of COX-1 in these cells [12]. This evidence concerns the gene PTGS1 and Hyperglycemia.