In cardiovascular disease, GAS5 exhibits three key protein interactions: binding to sema3a to reduce cardiac damage and apoptosis following myocardial infarction [136], interacting with Annexin A2 to regulate smooth muscle cell activity and maintain vascular homeostasis in varicose veins [139], and binding to Smad3 to act as a molecular brake on TGF-β signaling in smooth muscle cell differentiation [140]. Here, GAS5 is linked to cardiovascular disorder.