The depletion of MDSCs induced by sunitinib seems to be mediated by the inhibition of VEGF, c-Kit and Stat3, which, when activated, promote various immunosuppressive mechanisms (e.g., blockade of DC maturation and release of IL-10) and the expression of angiogenic and metastatic factors, inducing cancer cell resistance to the apoptotic activity of cytotoxic T cells [70,71]. This evidence concerns the gene VEGFA and cancer.