The moderate elevation of homocysteine (29 μmol/L), the coexistence of the PAI-1 4G/5G and ACE DD genotypes, and the presence of Factor V Leiden together likely collectively amplified thrombotic susceptibility through an intricate interplay of endothelial dysfunction, impaired fibrinolysis, and sustained hypercoagulability. Here, F5 is linked to endothelial dysfunction.