In vascular atherosclerotic lesions, radiation induced neovascularization enhances plaque growth, instability, and rupture through the contributing factors including ROS, inflammation, oxidized lipids, and metalloproteases like MMP-9.[22] Vascular smooth muscle cells (VSMCs) also secrete vascular endothelial growth factor (VEGF), vital for neovascularization and linked to atherosclerotic plaque destabilization.[23] Intraplaque hypoxia, a potent angiogenesis stimulator, can exacerbate lesions, induce intraplaque hemorrhage, and amplify oxidative and inflammatory responses.[16]. Here, VEGFA is linked to Atherosclerotic lesion.