Cardiovascular toxicity associated with anti-VEGF agents has become a major risk in cancer treatment, where suppression of VEGF expression, through alterations in Nitric Oxyde (NO) suppression and endotheline-1 (ET-1) stimulation, determines endothelial dysfunction and vasoconstriction, leading to is the main reason for hypertension. This evidence concerns the gene VEGFA and hypertensive disorder.