From this standpoint, the antitumor mechanism of lenvatinib administered after ICI therapy could be, at least partially, attributed to the targeting of the immunosuppressive cells expressing VEGF receptors and the restoring of the residual anti-PD-1/PD-L1 antibody function of antitumor CD8+ cells, in addition to the targeting of tumor cells [51]. This evidence concerns the gene CD274 and neoplasm.