Thus, overexpressed or specific tumor vessel molecules are better options as vascular direct ligand disruption targets, such as VEGFR2, Endomucin, Endoglin, MCAM, CD276, PSMA, ESM1, Fibrilin2, Emilin2, Lox, Serpin1, Sox17 or CD40 [96,97,98]. The gene discussed is KDR; the disease is neoplasm.