The article by Kamba and McDonald reviews the adverse effects of anti-VEGF therapy in cancer treatment, focusing on the mechanisms behind these side effects. Anti-VEGF agents, such as bevacizumab, sunitinib, and sorafenib, are widely used to inhibit vascular endothelial growth factor (VEGF) signaling, which is crucial for angiogenesis and tumor growth. However, these agents can also cause vascular disturbances and regression in normal organs, leading to various adverse events. Key adverse effects include hypertension, proteinuria, impaired wound healing, gastrointestinal perforation, hemorrhage, thrombosis, and cardiac impairment. These effects are often manageable but can be life-threatening in some cases. Preclinical studies in mice have shown that VEGF signaling is essential for the survival and plasticity of normal blood vessels, and its inhibition can lead to capillary regression in organs like the thyroid, pancreas, and renal glomerulus. The authors highlight the importance of understanding the underlying mechanisms of these adverse effects, optimizing dosing, and monitoring drug actions to improve patient safety and efficacy. They also discuss the potential for VEGF inhibitors to target specific organs or pathways, which could help reduce side effects and improve therapeutic outcomes.The article by Kamba and McDonald reviews the adverse effects of anti-VEGF therapy in cancer treatment, focusing on the mechanisms behind these side effects. Anti-VEGF agents, such as bevacizumab, sunitinib, and sorafenib, are widely used to inhibit vascular endothelial growth factor (VEGF) signaling, which is crucial for angiogenesis and tumor growth. However, these agents can also cause vascular disturbances and regression in normal organs, leading to various adverse events. Key adverse effects include hypertension, proteinuria, impaired wound healing, gastrointestinal perforation, hemorrhage, thrombosis, and cardiac impairment. These effects are often manageable but can be life-threatening in some cases. Preclinical studies in mice have shown that VEGF signaling is essential for the survival and plasticity of normal blood vessels, and its inhibition can lead to capillary regression in organs like the thyroid, pancreas, and renal glomerulus. The authors highlight the importance of understanding the underlying mechanisms of these adverse effects, optimizing dosing, and monitoring drug actions to improve patient safety and efficacy. They also discuss the potential for VEGF inhibitors to target specific organs or pathways, which could help reduce side effects and improve therapeutic outcomes.