VEGF-A is a multifunctional cytokine originally described for its ability to increase endothelial permeability, and subsequently reported to have critical roles in vascular development and cancer angiogenesis.7 We previously reported that HCV infection promotes VEGF-A expression, resulting in hepatocyte depolarization and enhanced viral entry.8–10 Treating HCV-infected hepatocytes with VEGF-A inhibitors, including sorafenib, restored their ability to polarize and limited viral infection,8,11 suggesting a therapeutic role for VEGF-A inhibitors in HCV infection. Here, VEGFA is linked to cancer.