The possible mechanism is that TACE induces hypoxia and promotes tumor angiogenesis to upregulate proangiogenic factors (VEGF and PDGF) and that the combination of sorafenib or lenvatinib treatment plays the largest antiangiogenic role by inhibiting the upregulation of proangiogenic factors following TACE in unresectable HCC. The gene discussed is VEGFA; the disease is neoplasm.