We speculated that the higher ORR in the TACE-Apatinib group could be associated with the fact that the affinity of Apatinib to VEGFR is tenfold of the affinity of Sorafenib to VEGFR, which could exert the effects through the VEGF pathway, inhibit the intracellular adenosine triphosphoric acid binding site of the VEGFR-2, reduce the tumor microvessel density, and promote the cell apoptosis [30, 31]. The gene discussed is KDR; the disease is neoplasm.