Several possible explanations exist for this finding (1) TACE can induce the up-regulation of VEGF and neovascularization, and apatinib can inhibit tumor angiogenesis by targeting VEGFR-2 (12); (2) TACE can cause tumor cell necrosis and neoangiogenesis, while the immune tolerance induced by TACE can be attenuated by TKI and PD-1 inhibitors (19, 20); and (3) the combination of ICIs with TKIs can convert “cold tumors” into “hot tumor” by T cell activation (11), which may restore exhausted T cells and facilitate anti-tumor immunity (21). Here, KDR is linked to neoplasm.