Learning Objectives After completing this course, the reader will be able to: Promptly recognize cardiovascular adverse events associated with anti‐VEGF therapy in order to formulate treatment plans to counteract them. Explain possible mechanisms by which bevacizumab, sunitinib, and sorafenib lead to cardiovascular complications and develop strategies for managing these complications. Describe the role of RAAS in vasoconstriction and capillary rarefaction and strategize the use of RAAS inhibition to manage these toxicities. This article is available for continuing medical education credit at CME.TheOncologist.com Background. Therapies targeting vascular endothelial growth factor (VEGF) are associated with hypertension, cardiotoxicity, and thromboembolic events. Methods. All prospective phase I–III clinical trials published up to December 2008 of approved anti‐VEGF therapies (bevacizumab, sunitinib, sorafenib) and relevant literature were reviewed. Results. The rates of Common Toxicity Criteria (version 3) grade 3–4 hypertension with bevacizumab, sunitinib, and sorafenib were 9.2%, 6.9%, and 7.2%, respectively. Grade 3–4 left ventricular systolic dysfunction was noted in 0.3%, 1.4%, and 0.05% of patients, respectively, whereas the rates of grade 3–4 thromboembolism were 9.6%, 1.2%, and 3.8%, respectively. The renin–angiotensin–aldosterone system (RAAS) may play a key role in vasoconstriction and capillary rarefaction, which are unleashed when VEGF signaling is targeted. Inhibiting RAAS may be the optimal approach for managing these toxicities. Conclusions. In anticipation of cardiovascular complications with anti‐VEGF therapies, early detection and personalized management may improve clinical outcomes and tolerance. This review focuses on the potential cardiovascular toxicities associated with the use of bevacizumab, sunitinib, and sorafenib in order to increase awareness about these complications and to discuss their clinical significance and therapeutic interventions.