The HLD triggers endothelial dysfunction characterized by an imbalance between vasodilation mediated by nitric oxide (NO) and prostacyclin-2 (PGI2) and vasoconstriction mediated by endothelin-1 (ET-1), causing abnormal responses that initiate atherosclerosis [31,32]; these implicate raised endothelial permeability, platelet aggregation, leukocyte adhesion, and cytokines release [31,32]. The gene discussed is EDN1; the disease is leukodystrophy.