Hyperglycemia induces endothelial dysfunction via multiple mechanisms: (1) impaired nitric oxide (NO) bioavailability, (2) enhanced thromboxane A2 (TXA2)‐mediated vasoconstriction, (3) oxidative stress driven by excessive reactive oxygen species (ROS) generation, and (4) release of proinflammatory cytokines such as IL‐6 and TNF‐α. This evidence concerns the gene IL6 and endothelial dysfunction.