Vascular endothelial growth factor (VEGF)-targeted therapies have been associated with thromboembolic events, although the magnitude and nature of this risk vary substantially according to the specific agent, mechanism of VEGF-pathway inhibition, malignancy, concomitant therapy, and patient-related factors. This comprehensive narrative review examines the epidemiology, mechanisms, clinical characteristics, and management of VTE in cancer patients receiving VEGF inhibitors. Evidence from clinical trials, observational studies, pharmacovigilance analyses, and preclinical investigations is synthesized to provide a clinically oriented overview of VEGF-targeted therapy-associated thrombosis. Reported VTE incidence ranges from 2.5% to 15.7% across studies, with substantial heterogeneity according to the VEGF-targeted agent, cancer type, treatment setting, and study design. Bevacizumab-treated patients receiving chemotherapy demonstrated increased arterial and venous thromboembolism risk (relative risk 1.32–2.45). Plasminogen activator inhibitor-1 (PAI-1) upregulation, endothelial dysfunction, and tissue factor activation represent key pathogenic mechanisms. Careful patient selection, risk stratification using validated scoring systems, thromboprophylaxis strategies, and individualized anticoagulation approaches are essential for managing this complication. Direct oral anticoagulants, particularly apixaban, demonstrate favorable efficacy and safety profiles compared to traditional anticoagulants in cancer-associated VTE. This review provides clinicians with comprehensive, evidence-based guidance for preventing and managing VTE in the growing population of cancer patients receiving VEGF-directed therapies.