Following aspirin administration, which irreversibly inhibits platelet COX-1, persistently elevated urinary 11dhTxB2 levels are thought to predominantly reflect TxA2 biosynthesis from non-platelet sources (e.g., via COX-2 or rapidly regenerated COX-1 in nucleated cells) [11,12], although the relative contributions pre-therapy in conditions like diabetes remain incompletely defined. This evidence concerns the gene PTGS1 and diabetes mellitus.