While sustained hyperglycemia induces endothelial dysfunction through reduced nitric oxide bioavailability, consistent with Chen et al. (28, 29) findings that endothelial dysfunction plays a key role in increasing cardiovascular risk in type 2 diabetes, participants with HbA1c levels of 6–13% would inevitably receive antidiabetic medications with modest blood pressure-lowering effects (SGLT2 inhibitors, GLP-1 agonists, DPP-4 inhibitors). The gene discussed is SLC5A2; the disease is Hyperglycemia.