* NRF2 downregulation * Anti-VEGF effect, ROS accumulation and disruption of NO levels and PI3K/Akt survival pathway. * Increased vasoconstriction due to disruption of both endothelium-dependent and -independent vasodilatation * Loss of pericytes due to inhibition of PDGF * Increased hematocrit and thrombogenesis activity by reducing NO- and PGI2-mediated anti-platelet activity * Atherosclerosis and increase in the risk of cholesterol embolization syndrome. This evidence concerns the gene AKT1 and atherosclerosis.