Since inhibition of GP73, the molecule that activates both VEGFA and VEGFR1/2/3 pathways, could effectively facilitate angiogenesis and decrease the risk of resistance induced by VEGF and VEGFR inhibitors, the pursuit of GP73-specific inhibitors mounts as a critical challenge in anti-angiogenesis therapy tailored to the TME of HCC. The gene discussed is FLT1; the disease is hepatocellular carcinoma.