Lenvatinib, a multi-target tyrosine kinase inhibitor (TKI), mediates its antitumor effects through dual mechanisms of vascular normalisation via potent inhibition of vascular endothelial growth factor receptors 1-3 (VEGFR1-3), which reduces tumour hypoxia and improves perfusion, and immune microenvironment remodelling through enhanced CD8+ T cell infiltration and reduced Treg cell accumulation.24 This evidence concerns the gene CD8A and neoplasm.