Moreover, endothelial dysfunction in FD was shown to be related to the activation of Endothelial Nitric Oxide Synthase (eNOS), directly or indirectly induced by GL3, which leads to increased activity of Inducible Nitric Oxide Synthase (iNOS) and Cyclooxygenase 2 (COX-2), with consequent overexpression of cell adhesion molecules such as ICAM-1, VCAM-1, and E-selectin [12]. Here, PTGS2 is linked to Fabry disease.