The rationale for combining these strategies lies in the following factors: (1) anti-PD-1 antibodies block inhibitory signals given by the interaction of PD-1 with its ligand, activating an immune response against tumors; (2) TACE induces devascularization of HCC and releases tumor-specific antigens [50,51]; and (3) targeting VEGF1–3, FGFR1–4, PDGFR a, RET and KIT, TKIs inhibit the pro-neoangiogenic and immunosuppressive effects of the tumor microenvironment [50,52,53]. This evidence concerns the gene FGFR1 and neoplasm.