The study of a CRC MCA26-bearing mouse model has shown that a multiple receptor tyrosine kinase-targeting inhibitor—sunitinib—could reduce the expression of IL-10, FOXP3, PD-1, CTLA-4, and BRAF, while increasing Th1 cytokine (IFN-γ), in isolated tumor-infiltrating lymphocytes, likely due to its function of blocking VEGF receptors. The gene discussed is FOXP3; the disease is neoplasm.