We hypothesize that polymicrobial infection disrupts endothelial function through reduced NO bioavailability, oxidative stress, inflammation, and impaired metabolic signaling, whereas treatment with either agent would restore endothelial integrity by re-establishing eNOS/BH4/NO coupling, activating Nrf2-mediated antioxidant defenses, and normalizing PI3K–AKT–IRS–GLUT signaling. The gene discussed is SLC2A1; the disease is infection.