Because sunitinib may inhibit different kinases dose dependently and withvariable potency, it is tempting to speculate that—at the highest doses tested inmice—it may have reversed its pro-metastatic activity by impairing STAT3-mediated survival ofearly-disseminated cancer cells, or by depleting metastasis-promoting, CSF1R-dependent inflammatorymonocytes. This evidence concerns the gene STAT3 and cancer.