High-dose VEGFR2-TKI treatment induced IL17A production by tumor-infiltrating γδ T cells through the VEGFR1-PI3K-AKT pathway, while IL17A promoted “N2” neutrophil polarization, driving immunosuppression and conferring resistance to anti-VEGFR2 treatment (Figure 8). This evidence concerns the gene AKT1 and neoplasm.